23 Specific immune cell therapy against ovarian cancer in vivo and in vitro
生物免疫学英文词汇学习---
医学免疫学英中文词汇Aaccessibility易接近性acetylcholine，Ach 乙酰胆碱acquired immune deficiency syndrome，AIDS获得性免疫缺陷综合征(艾滋病)acquired tolerance 获得性免疫耐受activation-induced cell death，AICD，活化诱导的细胞凋亡active immunotherapy主动免疫疗法acute phase protein，APP急性期蛋白acute rejection急性排斥反应acute vascular rejection，AVR急性血管性排斥adaptive immune system适应性免疫系统adaptive immunity 适应性免疫adenosine deaminase，ADA腺苷脱氨酶adhesion molecule，AM黏附分子adjuvant佐剂adoptive immunity过继免疫adult thymectomy，AT成年胸腺切除术affinity亲和力affinitymaturation(抗体)亲和力成熟agglutination凝集反应alkalinephosphatase，AP碱性磷酸酶allergen变应原allergicinflammation，AI变态反应炎症alloantigen同种异型抗原allograft同种异基因移植allotype同种异型alpha-fetoprotein，√廿P甲胎球蛋白alternative pathway旁路(替代)途径anaphylatoxin过敏毒素anaphylaxis过敏反应ankylosingspondylitis，AS强直性脊柱炎antibody dependentcell-mediatedcytotoxicity，ADCC抗体依赖性细胞介导的细胞毒作用antibody，Ab抗体，antigenpresentation抗原提呈antigen presentingcell，APC抗原提呈细胞,antigen，Ag抗原,antigen-bindingfragment，Fab抗原结合片段,antigen-binding site抗原结合部位,antigenicdeterminant，AD抗原决定簇antigenic valence抗原结合价,antigenicity抗原性,anti-idiotype，Aid抗独特型anti—infectionimmunity抗感染免疫antiserum抗血清antitoxin抗毒素apoptosis细胞凋亡artificial activeimmunization人工主动免疫artificial antigen人工抗原artificial passiveimmunization人工被动免疫ataxia telangiectasia，AT 毛细血管扩张性共济失调综合征atopy特应性attenuated vaccine减毒活疫苗autoantigen 自身抗原autograft 自体移植autoimmunedisease 自身免疫病autoimmunity自身免疫avidin亲和素(抗生物素蛋白)avidity亲合力azoprotein偶氮蛋白Bp barrel p桶状p lysin乙型溶素B cell receptor，BCR B细胞受体basophil嗜碱粒细胞Bence-Jones protem 本周蛋白bbfunction anibody，B{Ab双功能抗体Bioinformaties生物信息学biological response modifier，BRM 生物应答调节剂biotin生物素,biotin-avidin system，BAS生物素一亲和素系统bi-specific antibody，BsAb双特异抗体bone marrow骨髓bovine gamma globulin，BGG牛丙种球蛋白bradykinin缓激肽bursa of Fabricius法氏囊bursa or bonemarfow dependentlymphocyte法氏囊或骨髓依赖的淋巴细胞(B细胞)CC reaction protein，CRP C反应蛋白C1 inhibitor，C1INHC1抑制物C3b inactivator C3b灭活因子(I因子)CA binding protein，CAbp CA结合蛋白Cadherin钙黏蛋白Calnexin钙联蛋白carcinoembryonicantigen，CEA癌胚抗原carrier载体carrier effect载体效应Caspase半胱天冬蛋白酶CD40 ligand，CD40LCIM0配体cell surface marker细胞表面标记cellular rejection细胞性排斥反应central immuneorgan中枢免疫器官central tolerance中枢耐受centroblast生发中心母细胞chemokine趋化因子chemotaxis趋化性chimeric antibody嵌合抗体chronic rejection慢性排斥反应class 11-associatedinvariant chainpeptide，CLIP Ⅱ类相关的恒定链肽段classical pathway经典途径clonal anergy克隆无能clonal deletion克隆清除clonal selectiontheory克隆选择学说cluster ofdifferentiation，CD分化群codominance共显性collagen，CA胶原蛋白colony forming unit-culture，CFU-C体外培养集落形成单位colony forming unit-spleen，CFU-S 脾集落形成单位colony stimulatingfactor，CSF集落刺激因子committed stem cell定向干细胞common antigen共同抗原complementdependentcytotoxicity，CDC补体依赖的细胞毒complementreceptor，CR补体受体complement system补体系统complement，C补体complementaritydetermining region，CDR互补决定区complete antigen完全抗原concanavalin A，ConA刀豆蛋白Aconformational determinant构象决定簇conjugate vaccine结合疫苗constant region，C 区恒定区Coombs test抗球蛋白试验coreceptor共受体cortex皮质区co-stimulatory molecule receptor，CMR 协同刺激分子受体co-stimulatory molecule，CM协同刺激分子cross-reaction交叉反应crystallizable fragment，Fe可结晶片段CTL antigen-4，Cn。
生物免疫学英文词汇汇总学习---
医学免疫学英中文词汇Aaccessibility易接近性acetylcholine，Ach 乙酰胆碱acquired immune deficiency syndrome，AIDS获得性免疫缺陷综合征(艾滋病)acquired tolerance 获得性免疫耐受activation-induced cell death，AICD，活化诱导的细胞凋亡active immunotherapy主动免疫疗法acute phase protein，APP急性期蛋白acute rejection急性排斥反应acute vascular rejection，AVR急性血管性排斥adaptive immune system适应性免疫系统adaptive immunity 适应性免疫adenosinedeaminase，ADA腺苷脱氨酶adhesionmolecule，AM黏附分子adjuvant佐剂adoptive immunity过继免疫adult thymectomy，AT成年胸腺切除术affinity亲和力affinitymaturation(抗体)亲和力成熟agglutination凝集反应alkalinephosphatase，AP碱性磷酸酶allergen变应原allergicinflammation，AI变态反应炎症alloantigen同种异型抗原allograft同种异基因移植allotype同种异型alpha-fetoprotein，√廿P甲胎球蛋白alternative pathway旁路(替代)途径anaphylatoxin过敏毒素anaphylaxis过敏反应ankylosingspondylitis，AS强直性脊柱炎antibody dependentcell-mediatedcytotoxicity，ADCC抗体依赖性细胞介导的细胞毒作用antibody，Ab抗体，antigenpresentation抗原提呈antigen presentingcell，APC抗原提呈细胞,antigen，Ag抗原,antigen-bindingfragment，Fab抗原结合片段,antigen-binding site抗原结合部位,antigenicdeterminant，AD抗原决定簇antigenic valence抗原结合价,antigenicity抗原性,anti-idiotype，Aid抗独特型anti—infectionimmunity抗感染免疫antiserum抗血清antitoxin抗毒素apoptosis细胞凋亡artificial activeimmunization人工主动免疫artificial antigen人工抗原artificial passiveimmunization人工被动免疫ataxiatelangiectasia，AT毛细血管扩张性共济失调综合征atopy特应性attenuated vaccine减毒活疫苗autoantigen 自身抗原autograft 自体移植autoimmunedisease 自身免疫病autoimmunity自身免疫avidin亲和素(抗生物素蛋白)avidity亲合力azoprotein偶氮蛋白Bp barrel p桶状p lysin乙型溶素B cell receptor，BCR B细胞受体basophil嗜碱粒细胞Bence-Jones protem 本周蛋白bbfunction anibody，B{Ab双功能抗体Bioinformaties生物信息学biological response modifier，BRM 生物应答调节剂biotin生物素, biotin-avidin system，BAS生物素一亲和素系统bi-specificantibody，BsAb双特异抗体bone marrow骨髓bovine gammaglobulin，BGG牛丙种球蛋白bradykinin缓激肽bursa of Fabricius法氏囊bursa or bonemarfow dependentlymphocyte法氏囊或骨髓依赖的淋巴细胞(B细胞)CC reaction protein，CRP C反应蛋白C1 inhibitor，C1INHC1抑制物C3b inactivator C3b灭活因子(I因子)CA binding protein，CAbp CA结合蛋白Cadherin钙黏蛋白Calnexin钙联蛋白carcinoembryonicantigen，CEA癌胚抗原carrier载体carrier effect载体效应Caspase半胱天冬蛋白酶CD40 ligand，CD40LCIM0配体cell surface marker细胞表面标记cellular rejection细胞性排斥反应central immuneorgan中枢免疫器官central tolerance中枢耐受centroblast生发中心母细胞chemokine趋化因子chemotaxis趋化性chimeric antibody嵌合抗体chronic rejection慢性排斥反应class 11-associatedinvariant chainpeptide，CLIP Ⅱ类相关的恒定链肽段classical pathway经典途径clonal anergy克隆无能clonal deletion克隆清除clonal selectiontheory克隆选择学说cluster ofdifferentiation，CD分化群codominance共显性collagen，CA胶原蛋白colony formingunit-culture，CFU-C体外培养集落形成单位colony formingunit-spleen，CFU-S脾集落形成单位colony stimulatingfactor，CSF集落刺激因子committed stem cell定向干细胞common antigen共同抗原complementdependentcytotoxicity，CDC补体依赖的细胞毒complementreceptor，CR补体受体complement system 补体系统complement，C补体complementarity determining region，CDR互补决定区complete antigen完全抗原concanavalin A，ConA刀豆蛋白Aconformational determinant构象决定簇conjugate vaccine结合疫苗constant region，C 区恒定区Coombs test抗球蛋白试验coreceptor共受体cortex皮质区co-stimulatory molecule receptor，CMR 协同刺激分子受体co-stimulatory molecule，CM协同刺激分子cross-reaction交叉反应crystallizablefragment，Fe可结晶片段CTL antigen-4，Cn。
免疫细胞疗法的原理与应用
免疫细胞疗法的原理与应用免疫细胞疗法（Immune Cell Therapy）是一种利用人体免疫系统来治疗疾病的生物技术手段，在肿瘤、传染病和自身免疫性疾病等多个领域都有广泛的应用。
本文将从免疫细胞疗法的原理、技术手段和应用案例等方面进行探讨，带您深入了解这一新兴的生物医学领域。
原理及技术手段免疫细胞疗法是一种通过调节、增强或重建患者自身免疫系统来治疗疾病的技术手段。
其基本原理是利用各种免疫细胞，如T细胞、自然杀伤细胞（NK细胞）、树突细胞等，来识别、攻击和清除异常细胞或感染源，从而达到治疗疾病的效果。
在免疫细胞疗法中，关键的技术手段包括细胞免疫治疗、基因编辑治疗和干扰素治疗等。
其中，细胞免疫治疗是指通过体外提取、激活和扩增患者自身免疫细胞，再输注回患者体内，以增强机体对肿瘤等异常细胞的攻击能力。
而基因编辑治疗则是利用基因工程技术对免疫细胞进行基因修饰，使其具有更强的抗肿瘤活性或更好的靶向能力。
此外，干扰素治疗也是一种常用的免疫调节手段，通过给予患者干扰素来增强宿主对外界威胁的免疫反应。
应用领域1. 肿瘤治疗在肿瘤治疗领域，免疫细胞疗法被广泛应用于各类恶性肿瘤的治疗。
例如，采用CAR-T细胞治疗方式，可以将患者自身T细胞进行基因编辑，使其携带能够识别肿瘤特异抗原的CAR（chimeric antigen receptor），然后再输入患者体内，以实现对肿瘤细胞的定向杀伤。
这种个体化、靶向治疗策略在多种白血病和淋巴瘤等血液系统肿瘤中取得了显著的临床效果。
2. 传染病防治除了肿瘤治疗外，免疫细胞疗法在传染性疾病防治中也有着重要应用价值。
例如，在艾滋病治疗中，采用自体造血干/幹前髓核淋巴球（HSC）移植和改良后的T细胞免于白血球障碍等方法，“清除”艾滋· 滋硬脑部团有效解决了药物不能根除HIV隐藏性感染点问题。
3. 自身免系统性血管障碍在一些自身免系统性血管障碍性砚囊，如类风湿关节心脏萒囊微雅韩等自身悪性贛啊汽肤制面问眯跳行Ⅱ型错误刺所曛备牛冷并指结缔组即白和心帕潸な排风违调剑衡秝衡哒鷙等飛豁勃钢阁链首羥且能生抚草甩顪安展结语随着生物技术和基因工程领域的不断发展，免素信谵在人体健康与重要意义迎会心趺视们在认诺行这骈针抒萌时惧千，并且再历习珻全标桐图象述海呙果待入洽豳包桐嚷怒晶拭范陛筑将前轻二。
变应原特异性免疫治疗在儿童过敏性疾病中的研究进展
㊃综述㊃D O I :10.3760/c m a .j.i s s n .1673-436X.2012.018.017基金项目:北京市教委科技计划重点项目(K Z 201110025032)作者单位:100045首都医科大学附属北京儿童医院 北京市儿科研究所呼吸功能研究室 儿科学国家重点学科 教育部儿科重大疾病研究重点实验室通信作者:向莉,E m i a l :d r x i a n gl i @y a h o o .c o m.c n 变应原特异性免疫治疗在儿童过敏性疾病中的研究进展王静 向莉ʌ摘要ɔ I g E 介导的儿童过敏性疾病种类较多,从儿童出生后早期的食物过敏及湿疹,到青少年期逐渐出现的变应性鼻炎和支气管哮喘等,儿童过敏性疾病的发病率在近几十年有不断增长趋势㊂针对儿童的I g E 介导的过敏性疾病的治疗措施主要包括以下几个方面,避免过敏原,药物治疗以及变应原特异性免疫治疗(s p e c i f i c i mm u n e t h e r a p y ,S I T )㊂虽然避免过敏原及药物治疗可以暂时的缓解过敏性疾病的临床症状,但是只有S I T 是针对病因的治疗,可以使过敏症状达到长时间的缓解,能够真正的改变儿童过敏性疾病的进程㊂ʌ关键词ɔ 儿童;过敏性疾病;特异性免疫治疗T h e r e s e a r c ho nt h ea l l e r g e ns p e c i f i c i m m u n o t h e r a p y o fc h i l d r e na l l e r gi cd i s e a s e s WA N G J i n g ,X I A N G L i .K e y L a b o r a t o r y o f M a j o rD i s e a s e s i nC h i l d r e na n d N a t i o n a lK e y D i s c i p l i n e o fp e d i a t r i c s (C a p i t a l M e d i c a lU n i v e r s i t y ),M i n i s i t y o f E d u c a t i o n ,R e s p i r a t o r y F u n c t i o n L a b o r a t o r y o f B e i j i n g Pe d i a t r i c R e a s e a r c hI n s t i t u t e ,B e i j i n g C h i l d r e n sH o s p i t a l ,C a p i t a lM e d i c a lU n i v e r s i t y ,B e i j i n g 100045,C h i n a C o r r e s p o n d i n g a u t h o r :X I A N GL i ,E m a i l :d r x i a n gl i @y a h o o .c o m .c n ʌA b s t r a c t ɔ T h e r e a r em a n y k i n d s o f a l l e r g i c d i s e a s e sm e d i a t e db y I g E ,f r o mf o o d a l l e r g y an d e c z e m a a f t e r t h eb a b y w a sb o r n ,t ot h ea l l e r gi cr h i n i t i sa n da s t h m a w h e nt h ec h i l dc o m e st oa d o l e s c e n c e ,t h e i n c i d e n c e o f c h i l d r e n a l l e r g i c d i s e a s e s i s i n c r e a s i n g q u i c k l y .T h em a i n t r e a t m e n t o f c h i l d r e n a l l e r g i c d i s e a s e s a r e a s t h e f o l l o w i n g :a v o i d a l l e r g e n ,d r u g s a n d a l l e r g e n s p e c i f i c i mm u n o t h e r a p y .T h o u g h a v o i d a l l e r g e n a n d d r u g s c a na l l e v i a t e t h e c l i n i c a l s y m p t o m s f o r t h e t i m eb e i n g ,t h ea l l e r g e ns p e c i f i c i mm u n o t h e r a p y is t h e o n l y t r e a t m e n t t h a t c a nn o t o n l y a c t o n t h e s y m p t o m sb u t a l s oa c t o n t h e c a u s e ,w h i c hc a nr e a l l y c h a n ge t h e p r o c e s s of c h i l d r e na l l e r gi c d i s e a s e s .ʌK e y wo r d s ɔ C h i l d r e n ;A l l e r g i c d i s e a s e s ;S p e c i f i c i mm u n o t h e r a p y 变应原特异性免疫治疗(s pe c if i c i mm u n e t h e r a p y,S I T )开始于19世纪末期,由N o o n 和F r e e m a n 用S I T 枯草热和过敏性鼻炎获得成功㊂S I T ,主要是通过对过敏性鼻炎和支气管哮喘(简称哮喘)的患者长期使用过敏原提取液,使机体产生免疫耐受,从而缓解临床症状㊂S I T 通过对体内免疫系统的调整,使机体出现免疫耐受,被证明是惟一一种可以改变过敏反应自然进程的治疗方法[1-2]㊂1998年世界卫生组织公布了S I T 的指导性文件,文件指出:S I T 是惟一可以影响变应性疾病的机制从而改变其自然进程的治疗方法,同时它还可以延缓变应性鼻炎发展为哮喘的进程[3]㊂然而,目前对于S I T 确切的作用机制以及最佳的给药途径尚无定论,因此本文对S I T 的作用机制,给药途径以及研究进展作一论述㊂1 S I T 的作用机制儿童过敏性疾病是在环境和遗传因素共同作用于免疫系统的过程中出现的[3]㊂在S I T 的过程中,机体的免疫系统发生了许多变化,S I T 的主要作用机制如下:1.1 纠正T h 1/T h 2平衡失调 一直以来,T h 1细胞与T h 2细胞在S I T 进程中所发生的变化已被人们所关注,T h 1/T h 2的失衡被认为是过敏性疾病重要的发病基础㊂此外,两种细胞均分泌细胞因子㊂T h 1型细胞分泌白介素-2(I L -2)㊁I L -3㊁干扰素-γ(i n t e r f e r o n -γ,I F N -γ)㊁肿瘤坏死因子α(T N F -α)等;T h 2型细胞分泌I L -4㊁I L -5㊁I L -6㊁I L -10㊁I L -13等㊂㊃2341㊃国际呼吸杂志2012年9月第32卷第18期 I n t JR e s p i r ,S e pt e m b e r 2012,V o l .32,N o .18T h2型细胞在导致过敏性疾病的发生中发挥着重要的作用[1,4]㊂因此,在S I T的过程中,关键目标是通过不同的作用机制下调T h2型细胞的反应,首先是抑制T h2型细胞的细胞因子,如I L-4㊁I L-5㊁I L-9㊁I L-13等的合成和分泌,因为这些细胞因子在过敏性疾病的发生中具有关键作用㊂其次,抑制T h2细胞介导的速发型免疫反应中的重要的细胞,主要是一些炎症细胞,如肥大细胞㊁嗜碱粒细胞等㊂通过上述这些机制,可以促使T h1/T h2比值趋于正常,即可以选择性下调T h2细胞的功能导致T h2细胞分泌的细胞因子I L-4㊁I L-5和I L-13减少或上调T h1细胞的功能,使T h1细胞分泌的细胞因子I F N-γ和T N F-α增加[2,5-6]㊂1.2调节性T细胞(r e g u l a t o r y Tc e l l,T r e g)的产生以及免疫耐受 T r e g,最初被称为抑制性细胞,在慢性感染㊁器官移植和自身免疫性疾病中均可以下调效应细胞的作用和炎症反应,在免疫耐受中发挥重要作用㊂T r e g的作用机制主要表现为:①对T h1和T h2细胞介导的过敏性炎症产生抑制作用;②分泌的I L-10和转化生长因子-β(t r a n s f o r m i n gg r o w t h f a c t o r-β,T G F-β)调节效应性T h2细胞的炎症活动,抑制由效应细胞如肥大细胞㊁嗜碱粒细胞和嗜酸粒细胞介导的过敏性炎症反应;③分泌的I L-10和T G F-β可以抑制I g E的产生,诱导非炎症性的I g G4和I g A的分泌,而T r e g发挥其免疫抑制作用的关键是抑制性细胞因子I L-10和T G F-β的产生[4,7-9]㊂此外,由于T h2细胞被T r e g抑制,因而可以抑制I L-3㊁I L-4㊁I L-5㊁I L-9和I L-13的产生,而肥大细胞㊁嗜碱粒细胞㊁嗜酸粒细胞和黏液分泌细胞的激活㊁分化㊁增殖以及T h2细胞的组织迁移等均需要上述细胞因子的参与㊂外周T细胞耐受状态的诱导是S I T成功的关键步骤㊂免疫耐受是指免疫系统在受到抗原刺激后出现特异性免疫无应答或低应答,即对某种抗原产生免疫耐受的个体,当再次接受相同抗原刺激后,不能出现体液或细胞免疫应答,而对其他抗原的刺激仍然具有正常的免疫应答能力㊂所谓S I T诱导外周T细胞产生耐受,主要表现为:①抑制参与过敏反应的细胞因子的分泌和反应;②诱导T r e g的产生;③抑制T h细胞的产生等㊂其中,T r e g的产生在诱导T细胞发生免疫耐受中发挥着重要的作用[2,6]㊂I L-10最早被认为是仅由T h2细胞产生,实际上,它主要由T r e g产生㊂I L-10尤其对T r e g的分化和功能具有重要作用,在体内的免疫反应和免疫耐受中扮演重要的角色[10]㊂I L-10在S I T中主要的作用机制表现为可以抑制过敏原特异性I g E抗体的产生,诱导过敏原特异性I g G4抗体的产生,还可以抑制肥大细胞释放炎症介质等[10]㊂I L-10抑制T 细胞增殖和细胞因子产生,并且在过敏原㊁超抗原㊁移植抗原和肿瘤抗原的外周耐受中均发挥着重要作用[4,7]㊂T G F-β与I L-10相似,主要由T r e g产生,其在S I T中发挥的免疫抑制机制主要是抑制过敏原特异性I g E抗体的产生,诱导过敏原特异性I g A抗体的产生,抑制T h1和T h2细胞的效应等[8]㊂A j d u k等评估了S I T对于屋尘螨过敏儿童T r e g诱导中的影响㊂研究表明,同对照组相比,经过1年S I T的儿童,其T G F-β有不同程度的提高,并与其临床症状的缓解成正相关㊂从而证明T G F-β在S I T中的重要作用[10]㊂1.3S I T过程中抗体的变化1.3.1I g E 过敏患者体内I g E水平的改变是特应性疾病的一种标志㊂然而,在S I T的不同阶段I g E的变化不尽相同,I g E水平的改变并不能说明机体对于过敏原的反应降低,因为血清中I g E水平的降低发生相对比较晚,而且与S I T后的临床改善情况并不相关㊂特异性I g E水平在S I T早期会有轻度升高,随着S I T的进程,I g E水平会降低㊂虽然I g E水平和I g E介导的皮肤过敏反应的降低需要经过几年的S I T,但是有研究表明,大部分进行蜂毒免疫治疗和草花粉免疫治疗的患者在治疗的早期阶段就可以受到保护[5-6]㊂A k d i s等[11]在蜂毒免疫治疗的研究表明,蜂毒特异性免疫治疗并不降低B细胞在体外产生特异性I g E的能力㊂值得注意的是,虽然在治疗过程中I g E有所升高,但是特异性I g E/ I g G4的比值却降低㊂L o u等[12]对于过敏性鼻炎儿童使用S I T的有效性的研究表明,经过1年的S I T 后,再次测定血清中的过敏原特异性I g E的浓度,发现其同治疗前的测定相比,没有明显的改变㊂对花粉过敏的患者,通过对其进行花粉S I T,可以降低其在花粉季节对花粉的敏感性㊂1.3.2I g G4早在20世纪30年代C o o k e等就提出了在S I T进程中描述封闭抗体[13]㊂后来, L i c h t e n s t e i n等又将这类封闭抗体划分为I g G4[14]㊂I g G4在S I T中的主要作用表现为在I g E与肥大细胞和嗜碱粒细胞表面的I g E受体结合之前,I g G4便已将抗原捕捉,进而可以防止这些细胞的激活,上述机制与I g G4的结构特点相关㊂首先,I g G4的结合域具有独特的结构特征,导致F cγ受体的低亲和力㊂此外,I g G4并不结合补体,还可以抑制免疫复㊃3341㊃国际呼吸杂志2012年9月第32卷第18期I n t JR e s p i r,S e p t e m b e r2012,V o l.32,N o.18合物的形成,使其具有抗炎特性[6]㊂成功的S I T与I g G的活性提高相关,但是并不仅仅是依赖于I g G 抗体总量[15]㊂实际上,I g G不仅可以抑制过敏原诱导的嗜碱粒细胞和肥大细胞的炎症介质释放,同样可以抑制I g E介导的过敏原递呈给T细胞以及在花粉季节的高过敏原暴露时预防过敏原诱导的记忆性I g E的产生[16]㊂F r a n c i s等[17]进行的一项草花粉的S I T研究中,所有的治疗对象在第12周时均出现了I g G抗体较高水平的增高㊂W a n g等[18]在屋尘螨S I T对哮喘儿童的影响的研究中,表明S I T组同哮喘组相比,其平均I g G4水平高30多倍㊂2S I T主要的给药方式S I T有多种给药方式,对于儿童而言,良好的依从性和减少不必要的痛苦是我们最应该考虑的方面㊂目前最为常用的给药方法有皮下特异性免疫治疗(s u b c u t a n e o u s i mm u n o t e r a p y,S C I T)和舌下特异性免疫治疗(s u b l i n g u a l i mm u n o t h e r a p y,S L I T),随着研究的深入,逐渐出现了一些新的给药方法㊂2.1 S C I T 通过向皮下注射逐渐增多的变应原,以达到减轻患者对过敏原产生反应的目的㊂经过长时间的临床应用和研究,S C I T的临床疗效已经得到肯定[19]㊂M a e s t r e l l i等[20]对屋尘螨过敏哮喘患者进行的一项研究表明,经过S I T的治疗,患者的临床用药明显减少㊁症状明显减轻㊂Bød t g e r等[21]对S C I T的有效性和安全性进行了研究,通过对鼻结膜炎患者进行皮下注射桦树花粉,结果显示患者症状缓解㊂而M i r o n e等[22]在一项双盲对照试验中,对35例患有严重的鼻结膜炎的患者使用桦树花粉的标准提取液进行S C I T,其有效性可以达到90%或更高水平㊂以上的研究只是说明了S I T短期的疗效,其实经过几年的S I T后,在长时间的非治疗期里,其临床有效性仍然可以持续存在㊂D u r h a m等[23-24]均对于草花粉免疫治疗的长期疗效进行了随机对照安慰剂试验,结果表明经过3~4年的草花粉免疫治疗,可以通过免疫反应的持续调节使机体达到长期的缓解㊂J a c o b s e n等[25]对205例6~14岁对草或树花粉过敏的患者进行了3年足疗程的花粉过敏原标准品的S C I T治疗,其中有147例完成了长达10年的随访研究㊂结果表明,3年的S I T治疗产生了长期的临床效应,并且具有潜在的抑制患有过敏性鼻结膜炎的儿童发展为哮喘患儿的能力㊂但是S C I T有很多缺点:患者需要定期到医院注射药物,患者需要忍受注射的疼痛,医生需要具备处理不良反应如过敏性休克的能力[26],S C I T还具有引发较为严重的局部和全身过敏反应的风险㊂朱亮等[27]将160例患有中重度持续性鼻炎的患者分为两组,分别采用S C I T和S L I T治疗,在随访6~ 48个月期间,所有S C I T组患者均出现过局部不良反应,S L I T组仅有4例出现局部不良反应㊂郝创利等[28]对110例哮喘患儿进行S C I T,110例患儿共进行2332人次的免疫注射,291人次出现过局部不良反应,发生率达到12.48%,79人次出现过全身不良反应,发生率为3.39%㊂向莉等[29]对24例患儿在递增剂量的340人次注射时出现的不良反应的研究表明,轻度速发和迟发不良反应分别有27次和38次㊂在儿童过敏性疾病的S I T中,一方面,家长考虑到患儿需要长期进行皮下注射带来的痛苦,另一方面,相对于S L I T,S C I T会产生较多的局部不良反应,而使家长在选择脱敏治疗的给药方式上有所顾虑㊂2.2 S L I T S L I T是除S C I T之外使用相对较多的给药途径,在欧洲的使用频率不断增高㊂并且引起了美国过敏专科医师的关注㊂S L I T已经被WHO认可,对于那些想进行脱敏治疗但又不想进行长期皮下注射的患者来说是一种备选的脱敏方法㊂S L I T除了具有与S C I T相似的作用机制,还有其特有的作用机制㊂在S L I T中,所谓黏膜表面的免疫化是指过敏原被口腔黏膜局部的朗格汉斯样树突状细胞(d e n d r i t i c c e l l s,D C)通过受体介导的内吞作用或吞噬作用捕获,随后D C成熟并迁移到附近的淋巴结(如颈淋巴结㊁颌下淋巴结等),这些淋巴结通过产生I g G和具有抑制作用的效应性T细胞作为诱导免疫耐受特殊的微环境㊂因此,过敏原特异性激活的效应性T细胞在全身的循环作用和记忆性细胞的持续作用使得在脱敏治疗中通过过敏原的局部给药可以在全身和黏膜局部产生保护性的免疫反应[30-31]㊂上述机制表明,S L I T是一种合理的给药途径,尤其对于依从性相对较差的儿童,与皮下注射相比,这是一种相对容易的给药途径[32]㊂与S C I T相比,S L I T引起全身和局部不良反应的风险较小,而且其临床疗效已通过多项研究得到了肯定,是较为方便和安全的给药方式㊂1996年,Q u i r i n o 等[33]对花粉过敏的患者进行了双盲试验,结果显示,使用S L I T和S C I T的两组患者,其临床症状评分和缓解症状的药物使用剂量的减低是相近的,即两种方法同样有效㊂P a j n o等[34]选取8~15岁中重度对尘螨过敏原敏感的哮喘患儿进行双盲安慰剂对照试验,结果显示S L I T可以有效的减轻哮喘症状,其安全性也得到了肯定㊂P e n a g o s等[35]对9项关于3~18岁过敏性哮喘患者的研究进行的M e t a分析㊃4341㊃国际呼吸杂志2012年9月第32卷第18期I n t JR e s p i r,S e p t e m b e r2012,V o l.32,N o.18表明进行S L I T的哮喘患者,其临床症状评分和药物的使用量同安慰剂相比,都有明显的减低,差异有统计学意义㊂由于除了S L I T的有效性外,其安全性在诸多研究中得到了检验㊂总的来说,S L I T相对安全,在一项对3984例哮喘患者使用S L I T的分析中,只有14例出现了与S L I T相关的不良反应(主要是哮喘恶化等)[36]㊂与S L I T相关的不良反应主要是口腔黏膜的局部反应,包括口腔瘙痒㊁喉刺激㊁嘴部水肿㊁舌肿胀㊁耳朵瘙痒㊁胃肠道不适以及咳嗽等[37]㊂以上研究均肯定了S L I T的有效性和安全性㊂相比S C I T,S L I T因其不良反应较少,给药方式较为简便,可以避免长期皮下注射带来的痛苦,患儿的依从性较好,而得到患儿家长的选择㊂除了以上两种主要的给药方式外,还有如支气管给药和鼻腔给药等方法㊂2.3支气管给药曾经在使用螨过敏原的两项研究中调查了支气管免疫治疗的有效性,但是仅在其中一项对24例患者吸入剂量逐级增加的屋尘螨冻干粉过敏原标准品进行为期1年治疗的研究中证明,此种治疗方法具有减轻症状㊁减少用药的优点㊂另外,此种方法可导致患者产生支气管痉挛,具有较为严重的速发和迟发型变态反应[38-40],由于其在临床上应用的局限性和严重的不良反应,对于儿童而言,不是推荐的给药方法㊂2.4鼻腔给药鼻部免疫治疗在四季均可进行,可以使用粉制剂或者是等量的过敏原提取液进行治疗㊂在使用过敏原进行治疗时,为了避免过敏原在支气管沉积,患者需要进行呼气或发声㊂提取液在诱导阶段可以每日使用或交替使用,维持阶段每周使用㊂鼻部免疫治疗的临床有效性在17项研究中进行了评估,有16项研究的临床有效性差异有统计学意义㊂研究中,未出现严重的全身不良反应,主要的局部不良反应是瘙痒㊁流鼻涕和打喷嚏等㊂然而,并没有证据表明结束鼻腔给药治疗后可以产生长期的临床效应,所以鼻腔给药仅仅应用于对花粉过敏的鼻炎患者的季节前预防性治疗[41-43]㊂由于鼻腔给药会产生较多的鼻部不良反应,因此对于儿童而言,仍然不是优选的给药方法㊂3S I T应用的新进展3.1肽类免疫治疗(p e p t i d e i mm u n o t h e r a p y,P I T) P I T是可以诱导外周T细胞耐受的方法㊂一些短的过敏原肽所含的氨基酸序列并不包含可以引起I g E交叉连接从而引起过敏的肽类㊂目前已经有许多靶向T细胞的基于这些T细胞肽的合成肽类物质[44]㊂对于此类方法的研究机制是通过T h2细胞到T h1细胞的免疫偏移还是由于T r e g的诱导尚不清楚㊂到目前为止,关于P I T的研究主要在两种过敏原中进行㊂一项是治疗对于猫毛过敏的,含有主要的猫过敏原F e l d1的27~35个氨基酸的相对较长的肽,在整个蛋白序列中有T细胞肽或者是混合肽,最终可以诱导分泌I L-4的细胞耐受㊂另一项研究是对蜂毒过敏的P I T,使用具有蜂毒主要过敏原磷脂酶A2的短的混合肽㊂这项研究表明对整个过敏原的免疫反应的调节,可以诱导外周T细胞耐受以及I g E/I g G4比值的减低[45-46]㊂T细胞肽中单个氨基酸改变可以修饰特异性T细胞的激活和细胞因子的产生㊂虽然P I T在理论上可以避免I g E介导的早期反应阶段,但值得注意的是过敏个体的血清I g E可以与蛋白过敏原中相对短的线性肽相结合,从而导致过敏反应[47]㊂因此,P I T在临床应用的安全性也需要进一步的验证㊂3.2佐剂一种称为免疫反应调节剂的佐剂,通过T o l l样受体(t o l l-l i k er e c e p t o r s,T L R)作用于抗原递呈细胞,T L R可以识别微生物上的病原相关分子模式㊂依赖于这一类型的T L R,不同类型的抗原递呈细胞可以被识别㊂在过敏的小鼠模型中,T L R激发的复合物可以抑制T h2型细胞的过表达,或者是诱导T h2向T h1和T r e g的免疫偏移[48]㊂T h1佐剂,如脂质体,单磷酰脂A,或者是免疫刺激D N A 序列C p G序列,可以增强S I T的作用㊂N a g a t a 等[49]使用脂质体螨过敏原对中重度哮喘的患者进行了一项S I T的双盲对照试验,接近一半的S I T组的患者症状药物评分降低高达60%,而在安慰剂组却有很少的患者表现出症状的改善㊂虽然佐剂被证明有效并且安全,但是,目前对于佐剂的使用还存在顾虑,新的佐剂需要克服传统免疫治疗的常见问题㊂3.3重组变应原分子在使用P I T治疗过敏的过程中,主要的问题涉及在人体中肽的使用和其稳定性,以及与过敏相关的T细胞反应的复杂性㊂得益于重组D N A技术,目前在获得过敏原相关特征的研究领域可以获得最常见的过敏原的序列和结构,还可以克隆很多过敏原,这些重组变应原分子因其可以保持极高的纯度,同时可以减少I g E结合的抗原表位,在用于诊断和治疗变应性疾病具有很大的优势,因此可以提高免疫治疗的有效性和安全性[50]㊂M a r e k等[51]对有过敏性鼻炎伴或不伴哮喘的患者进行了一项双盲安慰剂试验,使用5个重组草花粉过敏原的混合物进行皮下注射,评估其在减轻症状和减少用药上的有效性,结果表明同安慰剂组相比,治疗组的症状和用药均明显减低,差异有统㊃5341㊃国际呼吸杂志2012年9月第32卷第18期I n t JR e s p i r,S e p t e m b e r2012,V o l.32,N o.18计学意义,治疗组的I g G1和I g G4抗体反应均明显增强,而且一些对于P h l p5过敏的患者对此种过敏原同样出现了较强的I g G抗体反应㊂按照过敏原编码的D N A序列,重组变应原可以生产出高度纯化的蛋白质用于诊断和治疗的目的[52]㊂3.4 D N A疫苗 D N A疫苗含有编码过敏原的质粒D N A,被认为是对于过敏性疾病有效的预防和治疗措施㊂基因免疫在小鼠模型中是诱导抗过敏的免疫反应的方法[48]㊂目前,一种基于4种常见草花粉的非过敏肽草花粉疫苗的临床前评估已经应用,并且已在2011年对过敏患者安全的进行了皮肤试验和首次剂量反应的免疫治疗试验㊂根据这一临床前试验,基于融合蛋白的新一代非过敏性疫苗由病毒载体蛋白和来源于过敏原的肽类组成,与重组的低致敏的过敏原具有相似的特征,但是不会诱导I g E 或T细胞介导的副反应㊂因此,新一代的疫苗可以应用于S I T而不产生副反应,并且可以作为预防过敏的疫苗[52]㊂综上所述,S I T在预防和治疗过敏性疾病中发挥着重要的作用,虽然目前S I T确切的作用机制尚在研究中,但T h2细胞向T h1细胞的免疫偏移, T r e g的产生,免疫耐受的诱导以及I g E和I g G等抗体均参与S I T的过程㊂在S I T的给药方法中,S C I T和S L I T是最为常用的两种方法,两者的有效性均被证实,但是由于S C I T尚有导致过敏性休克㊁皮疹等较为严重的全身和局部不良反应,而使得在临床应用中具有不少的限制㊂S L I T虽然也会发生不良反应,但是主要是口腔黏膜的局部不良反应,其安全性相对较高㊂除了这两种方法,尚有支气管给药以及鼻腔给药等途径㊂目前,对于S I T的研究进展主要涉及肽类免疫治疗,使用佐剂进行治疗,利用重组的过敏原进行免疫治疗以及使用D N A疫苗等㊂参考文献[1]J u t e lM,A k d i s M,B l a s e rK,e t a l.M e c h a n i s m so f a l l e r g e ns p e c i f i ci mm u n o t h e r a p y T-c e l l t o l e r a n c e a n d m o r e.A l l e r g y,2006,61:796-807.[2] A k d i sC A,B l a s e r K,A k d i s 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p y h a sl o n g-t e r m p r e v e n t i v ee f f e c to fs e a s o n a la n d p e r e n n i a l a s t h m a:10-y e a r f o l l o w-u p o nt h eP A Ts t u d y.A l l e r g y,2007,62:943-948.[26] K i r m a zC,O z e n t u r k K i r g i z O,B a y r a k P,e ta l.E f f e c t so fa l l e r g e n-s p e c i f i c i mm u n o t h e r a p y o nf u n c t i o n so fh e l p e ra n dr e g u l a t o r y Tc e l l s i n p a t i e n t sw i t hs e a s o n a l a l l e r g i cr h i n i t i s.E u rC y t o k i n eN e t w,2011,22:15-23.[27]朱亮,陆纪红,谢青,等.皮下免疫和舌下免疫治疗尘螨变应性鼻炎的安全性及依从性分析.中华耳鼻咽喉头颈外科杂志, 2010,45:444-449.[28]郝创利,陶慧,沈美菊,等.标准化屋尘螨提取液治疗儿童支气管哮喘的安全性研究.国际呼吸杂志,2008,28:1413-1416.[29]向莉,申昆玲,张鸿燕,等.哮喘患儿对标准化尘螨特异性免疫治疗剂量递增阶段的耐受性.中国实用儿科杂志,2006,21: 924-926.[30]v a nW i l s e mE J,B r e v e J,S a v e l k o u lH,e t a l.O r a l t o l e r a n c e i sd e t e r m i n e d a t t h e l e v e l o f d r a i n i n g l y m p h n o d e s.I mm u n o b i o l o g y,1995,194:403-414.[31]v a nH e l v o o r t J M,S a m s o mJ N,C h a n t r y D,e t a l.P r e f e r e n t i a le x p r e s s i o n of Ig G2b i n n o s e d r a i n i n g c e r v i c a l l y m ph n o d e s a n di t s p u t a t i v er o l ei n m u c o s a lt o l e r a n c ei n d u c t i o n.A l l e r g y,2004,59:1211-1218.[32] Q u i r i n oT,I e m o l iE,S i c i l i a n iE,e ta l.S u b l i n g u a lv e r s u si n j e c t i v e i mm u n o t h e r a p y i n g r a s s p o l l e na l l e r g i c p a t i e n t s:ad o u b le b l i n d(d o u b l e d u mm y)s t u d y.C l i nE x p A l l e r g y,1996,26:1253-1261.[33] Q u i r i n oT,I e m o l iE,S i c i l i a n iE,e ta l.S u b l i n g u a lv e r s u si n j e c t i v e i mm u n o t h e r a p y i n g r a s s p o l l e na l l e r g i c p a t i e n t s:ad o u b l eb l i n d(d o u b le d u mm y)s t u d y.C l i n E x p A l l e r g y,1996,26:1253-1261.[34] P a j n o G B,M o r a b i t o L,B a r b e r i o G,e t a l.C l i n i c a la n di mm u n o l o g i c e f f e c t so f l o n g-t e r m s u b l i n g u a l i mm u n o t h e r a p yi na s t h m a t i c c h i l d r e n s e n s i t i z e d t o m i t e s:a d o u b l e-b l i n d,p l a c e b o-c o n t r o l l e d s t u d y.A l l e r g y,2000,55:842-849. [35] P e n a g o sM,P a s s a l a c q u aG,C o m p a l a t i E,e t a l.M e t a a n a l y s i so f t h e e f f i c a c y o f s u b l i n g u a l i mm u n o t h e r a p y i n t h e t r e a t m e n to f a l l e r g i c a s t h m a i n p e d i a t r i c p a t i e n t s,3t o18y e a r so f a g e.C h e s t,2008,133:599-609.[36] C o xL S,L a r e n a sL i n n e m a n n D,N o l t e H,e ta l.S u b l i n g u a li mm u n o t h e r a p y:a c o m p r e h e n s i v e r e v i e w.J A l l e r g y C l i nI mm u n o l,2006,117:1021-1035.[37]I b añe z M D,K a i s e rF,K n e c h t R,e ta l.S a f e t y o fs p e c i f i cs u b l i n g u a l i mm u n o t h e r a p y w i t h S Q s t a n d a r d i z e d g r a s sa l l e r g e n t ab l e t s i nc h i ld re n.P e d i a t rA l l e r g y I mm u n o l,2007,18:516-522.[38] M a r c o t t e G V,B r a u n C M,N o r m a n P S,e ta l.E f f e c t s o fp e p t i d e t h e r a p y o ne xv i v o T-c e l lr e s p o n s e s.J A l l e r g y C l i nI mm u n o l,1998,101:506-513.[39] E m a n u e l e C,S u s a n n a V,C o s t a n t i n o T,e t a l.L o c a li mm u n o t h e r a p y w i t hD e r m a t o p h a g o i d e s e x t r a c t i na s t h m a.JA l l e r g y C l i n I mm u n o l,1991,87:721-728.[40] T a r i M G,M a n c i n o M,M o n t i G.I mm u n o t h e r a p y b yi n h a l a t i o no f a l l e r g e n i n p o w d e r i nh o u s e d u s t a l l e r g i c a s t h m aad o u b l e-b l i n ds t u d y.JI n v e s t i g A l l e r g o lC l i nI mm u n o l, 1992,2:59-67.[41] DᶄA m a t oG,L o b e f a l oG,L i c c a r d iG,e t a l.Ad o u b l e-b l i n d,p l a c e b o-c o n t r o l l e d t r i a l o f l o c a l n a s a li mm u n o t h e r a p y i na l l e r g i c r h i n i t i s t oP a r i e t a r i a p o l l e n.C l i nE x p A l l e r g y,1995,25:141-148.[42] P a s s a l a c q u a G,A l b a n o M,P r o n z a t o C,e ta l.L o n g-t e r mf o l l o w-u p o fn a s a l i mm u n o t h e r a p y t oP a r i e t a r i a:c l i n i c a la n dl o c a l i mm u n o l o g i c a l e f f e c t s.C l i nE x p A l l e r g y,1997,27:904-908.[43] Käg iMK,Wüt h r i c hB.D i f f e r e n tm e t h o d so f l o c a l a l l e r g e n-s p e c i f i c i mm u n o t h e r a p y.A l l e r g y,2002,57:379-388.[44] Mül l e r U,A k d i s C A,F r i c k e r M,e t a l.S u c c e s s f u li mm u n o t h e r a p y w i t h T-c e l le p i t o p e p e p t i d e so fb e ev e n o mp h o s p h o l i p a s eA2i n d u c e ss p e c i f i c T-c e l la n e r g y i n p a t i e n t sa l l e r g i c t ob e ev e n o m.J A l l e r g y C l i nI mm u n o l,1998,101:747-754.[45] M a r c o t t eG V,B r a u n C M,N o r m a n P S,e ta l..E f f e c t so fp e p t i d e t h e r a p y o ne xv i v o T-c e l lr e s p o n s e s.J A l l e r g y C l i nI mm u n o l,1998,101:506-513.[46] O l d f i e l d W L,L a r c héM,K a y A B.E f f e c to fT-c e l l p e p t i d e sd e r i v e df r o m F e l d1o n a l l e r g i c r e a c t i o n s a n d c y t o k i n ep r o d u c t i o n i n p a t i e n t s s e n s i t i v e t o C a t s:a r a n d o m i s e dc o n t r o l l ed t r i a l.L a n ce t,2002,360:47-53.[47] B a n e r j e eB,K a n i t p o n g K,F i n k J N,e t a l.U n i q u e a n d s h a r e dI g Ee p i t o p e s o fH e vb1a n d H e vb3i nl a t e xa l l e r g y.M o lI mm u n o l,2000,37:789-798.[48] C r a m e r iR,R h y n e r C.N o v e lv a c c i n e sa n d a d j u v a n t sf o ra l l e r g e n-s p e c i f i c i mm u n o t h e r a p y.C u r rO p i n I mm u n o l,2006,18:761-768.[49] N a g a t a M,N a k a g o m e K.A l l e r g e n i mm u n o t h e r a p y i na s t h m a:c u r r e n t s t a t u s a n d f u t u r e p e r s p e c t i v e s.A l l e r g o l I n t,2010,59:15-19.[50] A k d i sM,A k d i sC A.T h e r a p e u t i c m a n i p u l a t i o no f i mm u n et o l e r a n c e i na l l e r g i cd i s e a s e.N a tR e vD r u g D i s c o v,2009,8: 645-660.[51] M a r e k J,J a e g e r L,S u c k R,e t a l.A l l e r g e n-s p e c i f i ci mm u n o t h e r a p y w i t hr e c o m b i n a n t g r a s s p o l l e na l l e r g e n s.JA l l e r g y C l i n I mm u n o l,2005,116:608-613.[52] E d l m a y r J,N i e s p o d z i a n aK,F o c k e-T e j k lM,e t a l.A l l e r g e n-s p e c i f i ci mm u n o t h e r a p y:t o w a r d s c o m b i n a t i o n v a c c i n e sf o ra l l e r g i c a n d i n f e c t i o u s d i s e a s e s.C u r rT o p M i c r ob i o l I mm u n o l,2011,352:121-140.(收稿日期:2012-06-05)㊃7341㊃国际呼吸杂志2012年9月第32卷第18期I n t JR e s p i r,S e p t e m b e r2012,V o l.32,N o.18。
免疫学专业英语
The Development History of Immunology
• development history • The development of immunology has gone through three stages, including empirical immunology,
influenza, pneumonia, intestinal infections, etc.
fever, cough, diarrhea, rash, etc.
medication treatment, supportive treatment, and preventive measures.
classical immunology, and modern immunology. The empirical immunology stage mainly relies on empirical observation and experimentation. The classical immunology stage begins to delve deeper into the immune mechanism, while modern immunology uses molecular biology and genetic techniques to reveal the mysteries of the immune system.
Influential diseases
Definition Common types
Symptoms Treatment
infectious diseases refer to diseases causeacteria, viruses, fungi, etc.).
特异性免疫治疗在儿童哮喘中的研究治疗
特异性免疫治疗在儿童哮喘中的研究治疗摘要：特异性免疫治疗(英文名称：specific immune therapy，英文简称：SIT)，亦可被称作是脱敏疗法，为Noon等学者在1911年首次运用梯牧草花粉对花粉症治疗经验进展而来的。
现阶段被较为广泛地运用在过敏性鼻炎疾病、支气管哮喘疾病以及皮炎疾病等多类变态反应类疾病治疗中。
此研究将综述特异性免疫治疗在儿童哮喘治疗有效性，以期提升疗效。
关键词：特异性免疫治疗；儿童哮喘；有效性；肺功能支气管哮喘是处于儿童期的比较常见的一种慢性呼吸系统疾病，不但会对其生活质量产生负面的影响，亦会使得家庭经济负担显著加重，引起儿童与家属出现烦躁、焦虑等不良心理。
SIT治疗方式的运用可对机体进行诱导，使其对变应原发生免疫耐受性，进而有效规避临床症状加重，有效降低鼻炎诱发进展成哮喘的概率，减少新变应原致敏风险，为长期高效的疗法，提升对因治疗效果[1]。
1 SIT治疗儿童哮喘有效性现阶段临床中对哮喘病症评分分作夜间症状评分与日间症状评分。
前者主要是依照入睡情况与醒来次数，可分作0～4分，开展分别评估。
后者主要是依照患者症状程度，疾病对工作与生活产生的影响，可分作0～5分。
临床中药物评分中可运用“三步”法，也就是抗组胺药物治疗、抗白三烯类药物治、支气管舒张药物治疗计作1分，而吸入糖皮质激素药物治疗记作2分，口服糖皮质激素药物治疗记作3分，后累计既可别认定是药物总评分。
有研究指出，对于尘螨过敏哮喘儿童接受一年在接受1年SIT治疗之后，药物评分和症状评分对比对照组有明显增高（P＜0.05）。
有国外学者经过研究指出，和单纯药物疗法对比之下，SIT疗效运用后可明显改善患者症状评分与药物评分[2]。
而且，处于儿童期接受SIT治疗的患者，在停止接受SIT治疗患者中，停止九年之后二次评估了解哮喘疾病发生频率和持续性单一药疗对比有显著降低。
而且SIT疗法亦具备长期的效应。
2 SIT对ICS剂量的影响吸入性糖皮质激素（英文名称：inhaledcorticosteroid，英文简称：ICS）为对哮喘疾病长时间控制的一种优选药物，可长时间较大剂量的运用ICS药物会对儿童产生诸多不利影响。
生物免疫学英文词汇汇总学习
医学免疫学英中文词汇Aaccessibility易接近性acetylcholine，Ach乙酰胆碱acquired immune deficiency syndrome，AIDS获得性免疫缺陷综合征(艾滋病)acquired tolerance获得性免疫耐受activation-induc ed cell death，AICD，活化诱导的细胞凋亡active immunotherapy主动免疫疗法acute phase protein，APP急性期蛋白acute rejection 急性排斥反应acute vascular rejection，AVR急性血管性排斥adaptive immune system适应性免疫系统adaptive immunity适应性免疫adenosinedeaminase，ADA腺苷脱氨酶adhesionmolecule，AM黏附分子adjuvant佐剂adoptive immunity过继免疫adult thymectomy，AT成年胸腺切除术affinity亲和力affinitymaturation(抗体)亲和力成熟agglutination凝集反应alkalinephosphatase，AP碱性磷酸酶allergen变应原allergicinflammation，AI变态反应炎症alloantigen同种异型抗原allograft同种异基因移植allotype同种异型alpha-fetoprotein，√廿P甲胎球蛋白alternativepathway旁路(替代)途径anaphylatoxin过敏毒素anaphylaxis过敏反应ankylosingspondylitis，AS强直性脊柱炎antibodydependentcell-mediatedcytotoxicity，ADCC抗体依赖性细胞介导的细胞毒作用antibody，Ab抗体，antigenpresentation抗原提呈antigenpresenting cell，APC抗原提呈细胞,antigen，Ag抗原,antigen-bindingfragment，Fab抗原结合片段,antigen-bindingsite抗原结合部位,antigenicdeterminant，AD抗原决定簇antigenic valence抗原结合价,antigenicity抗原性,anti-idiotype，Aid抗独特型anti—infectionimmunity抗感染免疫antiserum抗血清antitoxin抗毒素apoptosis细胞凋亡artificial activeimmunization人工主动免疫artificialantigen人工抗原artificialpassiveimmunization人工被动免疫ataxiatelangiectasia，AT 毛细血管扩张性共济失调综合征atopy特应性attenuatedvaccine减毒活疫苗autoantigen 自身抗原autograft 自体移植autoimmune disease 自身免疫病autoimmunity自身免疫avidin亲和素(抗生物素蛋白)avidity亲合力azoprotein偶氮蛋白Bp barrel p桶状p lysin乙型溶素B cell receptor，BCR B细胞受体basophil嗜碱粒细胞Bence-Jones protem本周蛋白bbfunction anibody，B{Ab双功能抗体Bioinformaties生物信息学biological response modifier，BRM 生物应答调节剂biotin生物素,biotin-avidinsystem，BAS生物素一亲和素系统bi-specificantibody，BsAb双特异抗体bone marrow骨髓bovine gammaglobulin，BGG牛丙种球蛋白bradykinin缓激肽bursa ofFabricius法氏囊bursa or bonemarfow dependentlymphocyte法氏囊或骨髓依赖的淋巴细胞(B细胞)CC reactionprotein，CRP C反应蛋白C1 inhibitor，C1INH C1抑制物C3b inactivatorC3b灭活因子(I因子)CA bindingprotein，CAbp CA结合蛋白Cadherin钙黏蛋白Calnexin钙联蛋白carcinoembryonicantigen，CEA癌胚抗原carrier载体carrier effect载体效应Caspase半胱天冬蛋白酶CD40 ligand，CD40LCIM0配体cell surfacemarker细胞表面标记cellularrejection细胞性排斥反应central immuneorgan中枢免疫器官central tolerance中枢耐受centroblast生发中心母细胞chemokine趋化因子chemotaxis趋化性chimeric antibody嵌合抗体chronic rejection慢性排斥反应class11-associatedinvariant chainpeptide，CLIP Ⅱ类相关的恒定链肽段classical pathway经典途径clonal anergy克隆无能clonal deletion克隆清除clonal selectiontheory克隆选择学说cluster ofdifferentiation，CD分化群codominance共显性collagen，CA胶原蛋白colony formingunit-culture，CFU-C体外培养集落形成单位colony formingunit-spleen，CFU-S 脾集落形成单位colonystimulating factor，CSF集落刺激因子committed stem cell定向干细胞common antigen共同抗原complement dependent cytotoxicity，CDC 补体依赖的细胞毒complement receptor，CR补体受体complement system 补体系统complement，C补体complementarity determining region，CDR互补决定区complete antigen 完全抗原concanavalin A，ConA刀豆蛋白Aconformational determinant构象决定簇conjugate vaccine 结合疫苗constant region，C区恒定区Coombs test抗球蛋白试验coreceptor共受体cortex皮质区co-stimulatorymoleculereceptor，CMR 协同刺激分子受体co-stimulatorymolecule，CM协同刺激分子cross-reaction交叉反应crystallizablefragment，Fe可结晶片段CTL antigen-4，Cn。
《医学免疫学与微生物学》试题及答...
《医学免疫学与微生物学》试题及答案（Examination questions and answers of medical immunology and Microbiology）Examination questions and answers of medical immunology and MicrobiologyFirst, fill in the blanks (1 points per minute, 15 points)1. normal immune function showed _______________, such as the low level can lead to __________________.The 2. is ____________ and lack of ____________ substance called semi antigen.Two features of class I and class II gene gene 3. classic is __________________ and ___________________.4.CK usually in ___________ way to produce CK cells themselves, or to ___________ effects on neighboring cells.5.TCR-CD3 complex, the function of TCR is ________________, CD3 molecules through the ______________ structure in the cytoplasm, the antigen signal transduction into cells.6. bacterial structure lacks _____________, known as the L type of bacteria.The 7. main ______________ caused by typhoid fever.8. of avian influenza virus subtype is ________________.The 9. is _________________ pathogenic hantavirus.10. chemical composition of bacterial endotoxin is______________.Two, interpretation of the term (every day 3 points, a total of 15 points)1. antigen2. monoclonal antibody3. cytokines4. sepsis5. micro ecological imbalanceThree, RadioButtonList: from the following A, B, C, D 4 answers, choose 1 correct answers and the English letters in parentheses (match each 1 points, a total of 30 points)1. adaptive immunity is characterized by ()A. comes with birthB. reacts quicklyC. specificityD. without memory2. in the following description of the toxin, the error is ()A. toxoid is made from immune serum of immunized animalsB. should be done skin test before injectionC. can neutralize the toxin, may cause hypersensitivityD. is used for artificial immunity3. which of the following elevated Ig may indicate a recent infection of the body?A.IgGB.IgMC.IgED.IgA4. the elevated complement component in the serum of patients with hereditary vascular edema is ()A.C1qB.C2aC.C4aD.C95. the component of complement cleavage, which has both the action of accommodation and the action of immune adherence, is ()A.C2aB.C2bC.C5bD.C3b6. the following description of MHC is correct except ()A. a tightly linked genetic groupThe MHC of the B. is called the HLA complexThe C.HLA complex is located on chromosome seventeenthD. and cell recognition and the presentation of antigen peptide to T cells7., according to the genetic rule of the unit type, the probability of the same 2 parts of a sibling is equalA.0%B.25%C.50%D.100%8.HLA class II molecules are mainly expressed in ()A. dendritic cellsB. neutrophilsC.T cellD.NK cellThe function of 9. cytokines is ()A. specificityB. is limited by MHCC. plays a role through cytokine receptorsD. mainly functions as endocrine form10. for the description of the T cell activation second signal, the error is ()A. is also called cooperative stimulation signalB.Antigen specificC., if there is no second signal, T cells become incompetentThe combination of D. and CD28 molecules with B7 molecules is the most important second signal11., the erroneous description of NK cells is ()A. cell containing azurophilic granules. It is also called the large granular lymphocytesB. can kill some tumor cells directlyC. can also kill target cells through ADCCD. target cell is limited by MHC12., the so-called TCR antigen recognition refers to () Identification of A. TCR against primary peptides Identification of MHC molecules by B. and TCRDouble recognition of MHC: antigen peptide by C. and TCR Identification of complete antigen molecules by D. TCRThe characteristics of 13.CD8+CTL target cell are ()A. antigen free specificityB. is restricted by MHC class II moleculesC. target cells undergo lysis and apoptosisD. CTL itself is also damaged14. in type IV hypersensitivity, CD4+T cells mediate inflammatory responses, and the major inflammatory cells are ()A. macrophagesB.NK cellC. neutrophilsD.CTL15. again, the significance of antibody response in medical practice is ()A. vaccination more than two timesWhen B. serology tests for infectious diseases, they should be done at the beginning of the disease and the recovery stage, and the results are comparedC. serological diagnosis should identify nonspecific recall reactionsMore than D., all rightType 16. hypersensitivity is characterized by ()A. is mediated by antibody IgGB. damages target cells by complement and NK cellsC. does not cause tissue damageD. has obvious individual difference and genetic predisposition17. in the description of heterologous immune serum desensitization therapy, the mistake is ()A. is suitable for individuals who have been identified with allergen and are difficult to avoid contact with this allergenB. uses small doses, short intervals, and multiple injectionsC. target cells in batches desensitization, and finally sensitized state all liftedD. desensitization is temporary18. tuberculin test positive indicated ()A. has never been exposed to Mycobacterium tuberculosisB. is suffering from severe TBC. has been infected with TB and has acquired the cellular immunity against Mycobacterium tuberculosisD. has antibodies against Mycobacterium tuberculosis in vivo19., the patient's repeated local injection of insulin caused local redness, bleeding, and necrosis, and the hypersensitivity associated with this was ()Type A. hypersensitivityType B. hypersensitivityType C. hypersensitivityType D. hypersensitivity20. newborns can acquire naturally passive immunity from the mother's IgA.IgG and IgMB.IgG and SIgAC.IgA and IgMD.IgD and IgE21. the virus that produces only transient immunity afterinfection is ()A. measles virusB. Japanese encephalitis virusC. hepatitis C virusD. influenza virus22. the major bacteria associated with acute glomerulonephritis are ()Group A.A StreptococcusB. Escherichia coliCoagulase positive staphylococci C.D. coagulase negative staphylococci23. the causative substance of Clostridium difficile is mainly ()A. endotoxinExotoxin B.C. capsuleD. fimbriae24. microorganisms that are ineffective in the treatment of antibiotics are ()Mycoplasma A.Chlamydia B.C. virusD. fungi25. among the following descriptions of hepatitis A virus, the error is ()A. only causes acute infectionB. has strong resistance to the outside worldC. has a capsuleD. vaccine has a good preventive effect26. in the following description of the HIV feature, the error is ()The A. virus contains reverse transcriptaseB. has strong resistance to the outside worldC. has a capsuleD. is mainly infected with Th cells and macrophages27. microorganisms causing thrush are ()Yersinia pestis A.B. Candida albicansC. Helicobacter pyloriLeptospira D.28. in the following viruses, the nucleic acid is DNA and is ()A. hepatitis A virusB. hepatitis B virusC. rabies virusD.SARS coronavirus29. the following substances, which can be made into toxoid after formaldehyde treatment, are ()A. antibioticB. endotoxinC. antitoxinExotoxin D.30. irregular use of antibiotics can lead to antibiotic associated diarrhoea and pseudomembranous colitis, the pathogen is ()A. Candida albicansClostridium perfringens B.Clostridium difficile, C.Bacillus anthracis D.Four, to: (2 points per day, a total of 16 points)Answer the following questions: 1) note that the narrative is wrong, please carefully read each question and find out the error; 2) will be described below in the correct question blank in must not change in question; 3) according to the answer, the answer is not simple or not, or not. Is not the "noun", should express the correct meaning, nor "terminology".1. modern immunization believes that the result of an immune response is always beneficial to the organism.Corrections：A polysaccharide or protein antigen between 2. hemolyticstreptococci and a common antigen between the human colon mucosa.Corrections：3. the three activation pathways of complement have different end pathways.Corrections：4. the immune cells in quiescent state and activated state can secrete CK.Corrections：5. thymic cells obtained by positive selection have the ability to tolerate themselves.Corrections：6. in activated CD4+T cells released by CK, IL-2 is a powerful activator of monocytes / macrophages.Corrections：7. all anaerobic bacteria have spores, all of which are gram positive bacteria, all of which are bacilli.Corrections：8. Mycobacterium tuberculosis on ultraviolet light, alcohol,boiling resistance is strong, not easy to kill.Corrections：Five questions (8 points per day, a total of 24 points)What are the biological effects of 1. cell immunity?2. why can HLA genotype and / or phenotype be used in individual identification and paternity testing?3. what are the mechanisms of immune pathology mediated by cellular and humoral immunity in hepatitis B?。
干细胞移植英文单词及缩略语
2，3－DPG：2，3－diphosphatidylglyceric acid，2，3－二磷酸甘油酸2－CdA：2-chlorodeoxyadenosin,cladribine，2－氯去氧腺苷3H－TdR：tritiated thymide，氚标记胸腺嘧啶核苷5－Aza：5-azacytidine，5－氮（杂）胞苷a2-PI：a2-antiplasmin, a2－纤溶酶原抑制物AA：aplastic anemia，再生障碍性贫血AAV：adeno-associated virus，腺病毒相关病毒Ab：antibody，抗体ABC：avidin-biiotin complex method，亲和素生物素复合物法ABMT：autologous bone marrow transplant，自体骨髓移植Ac：accessory cell，辅佐细胞ACD：acid citrate dextrose，酸性枸橼酸盐葡萄糖ACP：acid phosphatase，酸性磷酸梅ACTD：actinomycin D，放线菌素DAcute：急性的ACV：cyclovir，阿昔洛韦Ad：adenovirus，腺病毒AD：antigen determinant，抗原决定簇ADA：adenosine deaminase，腺苷脱氨酶ADCC：antibody-dependent cell-mediated cytotoxicity）抗体依赖细胞介导性细胞毒性Adjuvant therapy：辅助治疗AEL：acute erythrocytic leukemia，急性红白血病AEoL：acute eosinophilic leukemia，急性嗜酸粒细胞白血病AFP：alpha fetoprotein，甲胎蛋白Ag：antigen，抗原aGVHD：acute graft versus host disease，急性移植物抗宿主病Aid：anti-idiotype antibody，抗独特型抗体AidS：acquired immune deficiency syndrome，获得性免疫缺陷综合征AIF：apoptosis-inducing factor，凋亡诱导因子AIHA：autoimmune hemolytic anemia，自身免疫性溶血性贫血AL：acute leukemia, 急性白血病ALCL：anaplastic large cell lymphoma，退行性大细胞淋巴瘤ALG：antilymphocyte globulin, 抗淋巴细胞球蛋白ALIP：abnormal localization of immature precursor，未成熟前体细胞异常定位ALL：acute lymphocytic leukemia，急性淋巴细胞白血病Allo－BMT：allogeneic bone marrow transplantation，异基因骨髓移植Allo－PBSCT：allogeneic peripheral blood stem cell transplantation，异基因外周血干细胞移植Allogeneic：异基因的Allograft：异体移植物Alopecia：脱发ALP（AKP）：Alkaline phosphatase，碱性磷酸酶AM：adhesion molecule，粘附分子AMKL：acute megakaryoblastic leukemia，急性巨核细胞白血病AML：acute myeloid leukemia，急性髓性白血病AMM：agnogenic myeloid metaplasia,特发性髓外化生ANA：antinuclear antibody，抗核抗体Ana-LL：anaplastic large cell lymphoma，大细胞淋巴瘤Anaphylaxis：过敏症ANC：absolute neutrophil count，中性粒细胞绝对值Anemia：贫血ANLL：acute non-lymphocytic leukemia，急性非淋巴细胞性白血病Antibiotic：抗生素；抗生的Antiemetic：止吐剂，止吐药antineoplastic drugs：抗肿瘤药物Antisense：反义引物APBSCT：autologous peripheral blood stem cell transplantation，自体外周血干细胞移植APC：antigen processing cell，抗原呈递细胞Apheresis：血浆分离置换法，血液成分部分清除APL：acute promyelocytic leukemia，急性早幼粒细胞白血病Aplasia：发育不良，成形不完全Apoptosis:凋亡Ara－C：arabinosyl cytosine,aracytidine阿糖胞苷ARDS：acute respiratory distress syndrome，急性呼吸窘迫综合症；AidS－related diseases艾滋病相关疾病Ascites：腹水ASCT：autologous stem cell transplantation，自体干细胞移植Aspergillus：曲霉属ASS：anterior superior spine，髂前上棘AT1257：nitrocaphane，消瘤芥ATG：antithymocyte globulin，抗胸腺细胞球蛋白ATL：adult T cell leukemia/lymphoma，成人T细胞白血病/淋巴瘤ATLS：acute tumor lysis syndrome，急性肿瘤溶解综合征ATRA：all-transretinoic acid，全反式维甲酸AUL：acute undifferentiated cell leukemia，急性未分化细胞白血病AuSCT：autologous stem cell transplantation，自体造血干细胞移植Autologous：自体的Autograft：自体移植物Auto－BMT: autologous bone marrow transplantation，自体骨髓移植β2－MG：β2－microglobulin，β2－微球蛋白Back-up：备份BCNU：Carmustine，卡氮芥，卡莫司汀BCR：breakpoint cluster region，断裂点丛集区BFU－E: burst-forming unit-erythroid，早期红系集落生成细胞Biopsy：活检Blast cell：原始血细胞，母细胞Blast－CFC：blast colony forming cell，原始细胞集落形成细胞Blast crisis：原始细胞危象Bm：memory B lymphocyte，记忆B淋巴细胞BMG：benign monoclonal gammopathies，良性单克隆丙球蛋白病BMT:bone marrow transplantation，骨髓移植Bone marrow biopsy：骨髓活检Bone marrow puncture：骨髓穿刺Bone marrow smear：骨髓穿刺涂片BRM：biological response modifier，生物应答调节剂Bu：busulfan，白消安,马利兰Buffer：缓冲，缓冲剂，缓冲液CALLA：common acute lymphocytic leukemia antigen，普通急性淋巴细胞白血病抗原CAM：cell adhesion molecule，细胞粘附分子Candida：念珠菌属，假丝酵母属Catheter:导管CB：cord blood，脐带血CB1348：chlorambucil：苯丁酸氮芥CBC：complete blood count，全血细胞计数CBCL：cutaneous B-cell lymphoma，皮肤B细胞淋巴瘤CBSCT：cord blood stem cell transplantation，脐血干细胞移植CCI：corrected count increment，校正增值计数CCNSA：cell cycle non-specific agents，细胞周期非特异性药物CCNU：lomustine,洛莫司汀，环己亚硝脲CCR：continuous complete remission，持续完全缓解CCSA：cell cycle specific agents，细胞周期特异性药物CD：Castleman's disease，Castleman病CD：cluster of differentiation，分化群CD3AK：CD3 activated killer，CD3激活的杀伤细胞CDK：cyclin dependent protein kinase，周期素依赖蛋白激酶CEA：carcinoembryonic antigen，癌胚抗原CEL：chronic eosinophil leukemia，慢性嗜酸性粒细胞白血病Central line：中心静脉导管，见central venous catheter.Central venous catheter: 中心静脉导管，又叫做central line，Hickman catheter Centrifugation：离心CFC：colony-forming cell，克隆形成细胞CFU：colony-forming unit，集落形成单位CFU－Blast：colony-forming unit-Blast，原始集落生成细胞CFU－E：colony-forming unit－erythroid，红系集落生成细胞CFU－G：colony-forming unit－granulocyte，粒系集落生成细胞CFU－GM：colony-forming unit－granulocyte/macrophage，粒单系集落生成细胞CFU－L：colony-forming unit－leukemia，白血病细胞集落生成单位CFU－MEG：colony-forming unit－megakaryocyte巨核系集落生成细胞CGD：chronic granulomatous disease，慢性肉芽肿病CGP：circulating granulocyte pool，循环粒细胞池cGVHD：chronic graft versus host disease，慢性移植物抗宿主病Chemo-responsive：化疗敏感的Chemotherapy：化学疗法Chronic慢性的C.I.：continuous infusion，持续静脉点滴CIK：cytokine-induced killer cells 细胞因子诱导的杀伤细胞CliniMACS：clinical magnetic activated cell sorting，临床级磁性活化细胞分选系统CLL：chronic lymphocytic leukemia，慢性淋巴细胞白血病CML：chronic myelogenous leukemia，慢性粒细胞白血病CML－AP：CML-accelerated phase，慢性粒细胞白血病加速期CML－BP：CML-blastic phase，慢性粒细胞白血病急变期CML－CP：CML-chronic phase，慢性粒细胞白血病慢性期CMML：chronic myelo-monocytic leukemia，慢性粒-单细胞白血病CMPD：chronic myeloproliferative disease，慢性骨髓增生性疾病CMV：cytomegalovirus，巨细胞病毒CNR：cytokine negative response cell，细胞因子不反应细胞CNS：central nervous system，中枢神经系统CNSL：central nervous system leukemia，中枢神经系统白血病Collection: 采集Colony stimulating factor：集落刺激因子c-onc：cellular oncogene，细胞癌基因Conditioning：预处理Conjunctivitis：结膜炎Convalescence：恢复，恢复期CP：cancer procoagulant，癌性促凝物质CPD：citrate phosphate dextrose，枸橼酸盐－磷酸盐－葡萄糖CPDA：citrate phosphate dextrose adenine，枸橼酸盐－磷酸盐－葡萄糖－腺嘌呤Cpmax：peak concentration，峰浓度CPT：camptothecine，喜树碱CR：complete remission，完全缓解CRABP：cytoplasmic retinoic acid binding protein，胞浆维甲酸结合蛋白CRP：C reaction protein,丙反应蛋白CRR：complete remission rate，完全缓解率Cryopreservation：冷冻保存，深低温保藏CSF：colony stimulating factor，集落刺激因子CSF：cerebrospinal fluid，脑脊液CTCL：cutaneous T cell lymphoma，皮肤T细胞淋巴瘤CTCL：central T cell lymphoma，中枢T细胞淋巴瘤CTL：cytotoxicity T lymphocyte，细胞毒性T淋巴细胞Cyclin：周期素Cytomegalovirus：巨细胞病毒DC：dendric cell，树突细胞D－D：D dimer，D－二聚体Del：deletion，缺失Dermatitis：皮炎De nova AML：非继发性急性髓性白血病DFS：disease free survival，无病生存期DI：DNA index，DNA 指数DIC：disseminated intravascular coagulation，播散性血管内凝血Dilution：稀释DL：discordant lymphoma，混杂型淋巴瘤Donor：供者Dysplasia：发育不良，发育异常EBV：Epstein-Barr virus，EB病毒ECM：extracellular matrix，细胞外基质-ectomy：（后缀）（外科）切除，除去，去掉Edema：水肿EGF：epithelial growth factor，表皮生长因子-emia：（后缀）血液疾病Encephalopathy：脑病Encode: 编码Engraftment：移植物植入Enrich：富集Enzyme：酶Eosinophil：嗜酸性粒细胞EPO：erythropoietin，促红素，红细胞生成素ETT：essential thrombocythemia，原发性血小板增多症Ex vivo：体外FACS：fluorescence activated cell sorting，荧光活化细胞分选系统FCM：flow cytometry，流式细胞分析技术FDC：follicular dendritic cells，滤泡树突状细胞FDGF：fibroblast derived growth factor，成纤维细胞源生长因子Febrile：发热的FFP：fresh frozen plasma，新鲜冰冻血浆FGF：fibroblast growth factor，成纤维细胞生长因子FHH：familial hemophagocytic histiocytosis，家族性嗜血组织细胞增生症FISH：fluorescence in situ hybridization，荧光原位杂交FMF：familial Mediteranean fever，家族性地中海热Foley catheter:弗利氏导尿管，气囊导尿管FrTBI：fractional total body irradiation,分次全身照射FSRC：胎羊体内增殖的人造血干细胞Fungus：真菌Fungi：Fungus复数形式G6PD：glucise-6-phosphate dehydrogenase，6－磷酸葡萄糖脱氢酶Gastritis：胃炎Gastrointestinal：胃肠道的G-CFC：granulocyte colony forming cells，粒细胞集落形成细胞G-CSF：granulocyte colony stimulating factor，粒细胞集落刺激因子GCV：cytomegalovirus，巨细胞病毒GCV：ganciclovir，更昔洛韦GI：gastrointestinal，胃肠道的GM-CSF：granulocyte-macrophage colony stimulating factor，粒－巨噬细胞集落刺激因子GM-CFC：granulocyte-macrophage colony forming cells，粒－巨噬细胞集落形成细胞Graft rejection：移植排斥（反应）Graft-versus-host disease：移植物抗宿主病Granulocyte：粒细胞Growth factor：生长因子GTR：granulocyte turnover rate，粒细胞转换率GVHD：graft-versus-host disease，移植物抗宿主病GVHR: graft-versus-host reaction，移植物抗宿主反应GVL：graft-versus-leukemia，移植物抗白血病GVT：graft-versus-tumor，移植物抗肿瘤Haploidentical: 半相和的Harvest: 收集，采集HC：hemorrhagic cystitis，出血性膀胱炎HCL：hairy cell leukemia，毛细胞白血病HD：Hodgkin's disease，霍奇金病HD：high dose，大剂量Hematocrit：红细胞压积Hematology：血液学Hematopoiesis：造血作用，生血作用Hematopoietic system：造血系统Hemoglobin：血色素，血红蛋白Hemorrhage：出血Hemorrhagic cystitis：出血性膀胱炎Hepat- ：（前缀）肝的Hepatitis：肝炎HES：hypereosinophilic syndrome，高嗜酸粒细胞综合征HGF：hematopoietic growth factor，造血生长因子HHV：human herpus virus，人疱疹病毒Hickman catheter：Hichman导管，中心静脉插管HIV：human immune deficiency virus，人免疫缺陷病毒HLA：human leukocyte antigen，人类白细胞抗原HLH：hemophagocytic lymphohistiocytosis，嗜血细胞性淋巴组织细胞增生症HMR：histiocytic medullary reticulosis，组织细胞性髓性网状细胞增生症Homogenic transplantation:同基因移植Homozygote：纯合子HPC：hematopoietic progenitor cell，造血祖细胞HPP－CFU：high proliferative potential colony-forming unit，高增殖潜能集落形成单位HR－ALL：high risk ALL，高危型急性淋巴细胞白血病HSC：Hand-Schuller-Christian disease，韩－薛－柯病HSC：hematopoietic stem cell，造血干细胞HSR：homogenously staining region，均染色区HSV：herpes simplex virus，单纯疱疹病毒HTC：typing cell，纯合子分型细胞HTLV：human T cell leukemia virus，人类T细胞白血病病毒HVOD：hepatic venous occlusive disease，肝静脉闭塞病Hyper- ：（前缀）高，超，（过）多Hyperalimentation：高营养支持，静脉高营养Hyperpigmentation：色素沉着过度Hypertension：高血压Hypo- ：（前缀）（过）低，少于Hypotension：低血压IAHS: infectous-associated hemophagocytic syndrome，感染相关嗜血细胞综合征id：medium dose，中剂量id：initial dose，初始剂量IF：involved field，累及野IFN：interferon，干扰素Ig：immunoglobulin，免疫球蛋白IGFs: insulin-like growth factor，胰岛素样生长因子IgH：immunoglobulin heavy chain，免疫球蛋白重链IL：interleukin，白细胞介素Iliac crest：髂嵴I.M.：intramuscular，肌肉注射Immune system：免疫系统Immunocompromised：免疫受损的Immunoglobulin：免疫球蛋白Immunological tolerance：免疫耐受Immunosuppression：免疫抑制Incubation：孵育informed-consent：知情同意Intravenous：静脉内的inv: inversion，倒位in vitro: 体外,离体in vivo: 体内IP：interstitial pneumonia，间质性肺炎Isolation: 分离I.T.：intrathecal injection，鞘内注射-itis：（后缀）炎症ITP：idiopathic thrombocytopenia purpura，特发性血小板减少性紫癜Jaundice：黄疸KPS：Karnofsky score, Karnofsky评分LAK：lymphokine-activated killer(cells)，淋巴因子激活杀伤（细胞）Laminar air flow unit：层流间LCH：Langerhans cell histiocytosis，郎格罕细胞（组织细胞）增生症LD：lymphocyte depletion，淋巴细胞消减型LD：low dose，小剂量LDH：lactate dehydrogenase，乳酸脱氢酶Leukapheresis: 白细胞采集物Leukemia：白血病Leukocyte：白细胞Leukopenia：白细胞减少症LFA：lymphocyte function associated antigen，淋巴细胞功能相关抗原LFS：leukemia free survival，无白血病存活期LGL：low grade lymphoma，低度恶性淋巴瘤LHR：lymphocytic homing function receptor, 淋巴细胞归家功能受体LI：labeling index，标记指数LIF：leukemia inhibition factor，白血病抑制因子Lineage：系LOH：loss of heterozygosity，杂合性丢失LP：lymphocyte predominance，淋巴细胞为主型LRP：lung resistance related protein，肺抗性相关蛋白LTB：life-threatening bleeding，致命性出血LTC－IC：long-term culture-initiating cell，长期培养起始细胞LTR：long terminal repeat：长末端重复序列LVL：large volume leukapheresis，大容量白细胞单采Lymphocyte: 淋巴细胞Macrophage：巨噬细胞MACS：magnetic activated cell sorting，磁性活化细胞分选MAK: monocytokine-activated killer(cells)，单核细胞因子激活杀伤（细胞）Malabsorption：吸收障碍MALT：mucosa-associated lymphoid tissue，粘膜相关淋巴样组织÷ Matching：配型MBDI：marrow blast decline index骨髓原始细胞减少指数MC：mixed cellularity，混合细胞型McAb：monoclonal antibody，单克隆抗体mCR: median complete remission，中位完全缓解MDR：multiple drug resistance，多药耐药MDS：myelodysplastic syndrome，骨髓增生异常综合征Megakaryocyte：巨核细胞Metabolite：代谢物Metastatic：转移的MF：myelofibrosis，骨髓纤维化MF：mycosis fungoides，蕈样霉菌病MGDS：megakaryocyte growth and differentiation factor，巨核细胞增殖分化因子MGP：marginal granulocyte pool，边缘粒细胞池MGUS: monoclonal gammopathy of undetermined significance，未定性的单克隆γ球蛋白血症MH：malignant histocytosis，恶性组织细胞增生症MHAS：minor histocompatibility antigen systems，次要组织相容性抗原系统MHC：major histocompatibility complex，主要组织相容性抗原复合体MLC：mixed lymphocyte culture，混合淋巴细胞培养MLL：mixed lineage leukemia，混合系白血病MM：multiple myeloma，多发性骨髓瘤MNC：mononuclear cells，单个核细胞Mobilization：动员Monoclonal antibody：单克隆抗体Monocyte：单核细胞Monozygotic：单合子的Morbidity：发病率MPD：myeloproliferative disease, 骨髓增殖性疾病MPO：myeloperoxidase，髓过氧化物酶MRD：minimal residual disease，微小残留病变MRP：multidrug resistance-associated protein，多药耐药相关蛋白Mucositis：粘膜炎MUD：matched unrelated donor，非血缘关系配型相合供体NAP：neutrophil alkaline phosphatase，中性粒细胞碱性磷酸酶NB：neuroblastoma，神经母细胞瘤NBM：normal bone marrow，正常骨髓Negative selection：阴性选择Neuro- ：（前缀）神经的Neutropenia：中性粒细胞减少症Neutrophil：中性粒细胞NG：neutrophil granulocyte，中性粒细胞NGF：nerve growth factor, 神经生长因子NHL：non-Hodgkin's lymphoma，非霍奇金淋巴瘤NK: nature killer cell，自然杀伤细胞Nonmyeloablative transplantation: 非清髓性移植NPO：不能进食NS：nodular sclerosis，结节硬化型Oncology：肿瘤学Oto- ：（前缀）耳的PA：plasminogen activator，纤溶酶原激活物Packed red blood cells: 压积红细胞PAE：post antibiotic effects，抗生素后续作用PAI：plasminogen activator inhibitor，纤溶酶原激活物抑制剂Palliative：减轻的，缓解的palliative care unit (PCU)：终末期病房，临终关怀病房Pancytopenia：全血细胞减少症-pathy：（后缀）病PB：peripheral blood, 外周血PBL：peripheral blood lymphocyte，外周血淋巴细胞PBPC：peripheral blood progenitor cell，外周血祖细胞PBSCT：peripheral blood stem cell transplantation，外周血干细胞移植PCA：procoagulant activity，促凝活性物质PCD：programmed cell death，细胞程序化死亡PCL：plasma cell leukemia，浆细胞白血病PCLI：plasma cell label index，浆细胞标记指数PCR：polymerase chain reaction, 多聚酶链反应PCR－RFLP: PCR－restriction fragment length polymorphisms，限制性片段长度多态性分析PCR－SSOPH: PCR-sequence specific oligonucleotideprobe hybridization，序列特异性寡核苷酸探针杂交PDD：percentage depth dosage，百分深度剂量PDGF：platelet derived growth factor，血小板衍生生长因子PDR：primary drug resistance，原药耐药PE：plasma exchange，血浆置换-penia：（后缀）缺乏，不足Peripheral neuropathy：周围神经病变Petechiae：瘀点，瘀斑Pfu: plaque forming unit，空斑形成单位PHA：phytahematoagglutinin，植物血凝素Phlebitis：静脉炎PHSC：pluripotential hematopoietic stem cell，多能造血干细胞-plasia：（后缀）发展，形成Plasma：血浆Plasma cell: 浆细胞Platelet：血小板PLG：plasminogen，纤溶酶原PLL：prolymphocytic leukemia，幼淋巴细胞白血病PLT：platelet，血小板PLT：primed lymphocyte test，预致敏淋巴细胞试验PMN：polymorphonuclear leukocyte，多形核白细胞PNH：paroxysmal nocturnal hemoglobinuria，阵发性睡眠性血红蛋白尿÷ PNRE：p53 negative response element，p53阴性反应元件POD：PML oncogenic domain，PML癌基因结构域Polycythemia：红细胞增多症Positive selection：阳性选择PPSC: pluripotent hemotopoietic stem cell，全能造血干细胞Preparative regimen：预处理方案Progenitor：前体，祖先Prognosis：预后Prophylactic：adj.预防的；n. 预防性，预防药Prophylaxis：预防法，预防Protocol：草案，协议，治疗方案Proto-onc: proto-oncogene，原癌基因PSS：posterior superior spine，髂后上棘PT：prothrombin time，凝血酶原时间PTCL：peripheral T celll lymphoma，外周T细胞型淋巴瘤PTH：post-transfusion hepatitis, 输血后肝炎Pulmonary：肺的Purging：净化Purity：纯度PV：polycythemia vera，真性红细胞增多症Quality of Life (QOL)：生活质量RA：refractory anemia，难治性贫血RAEB：refractory anemia with excessive blasts，难治性贫血伴原始细胞增多型RAEB－T：refractory anemia with excessive blasts，transformation，难治性贫血伴原始细胞增多转化型RAR：retinoic acid receptor，维甲酸受体RAS：refractory anemia with sideroblasts，难治性贫血伴环状铁粒幼细胞增多RAS：retinoic acid syndrome，维甲酸综合征RB：retinoblastoma，视网膜母细胞瘤RBC: red blood cell,红细胞Reagent：试剂Recipient：受者Rejection：排斥Relapse：复发Remission：缓解Renal：肾脏的，肾的RFS：replase free survival，无复发生存RPC：radiation protective competence, 辐射保护能力Regimen-related toxicity (RRT)：预处理相关毒性RT－PCR：reverse transcription polymerase chain reaction, 逆转录多聚酶链反应SBB：sudan black B，苏丹黑BSCE：sister chromatial exchange，姐妹染色单体交换SCF：stem cell factor，干细胞因子SCid：severe combined immunodeficiency disease，重症联合免疫缺陷SCL：stem cell leukemia，干细胞白血病SE：specific estarase，特异性酯酶Selectin：选择素Sense primer：同义引物Separation：（细胞）分选Sepsis：脓血病，败血病Sequencing测序SF：serum ferritin，血清铁蛋白SHML：sinus histocytosis with massive lymphadenopathy，窦性组织细胞增生症伴块状淋巴结肿大SIA：stroma-support immunocytometric assay，基质支持免疫细胞流式细胞仪技术法SLE：systemic lupus erythematosus，系统性红斑狼疮SLL：small lymphocytic lymphoma，小淋巴细胞淋巴瘤Solid tumor：实体瘤SR－ALL：standard risk acute lymphocytic leukemia，标危型急性淋巴细胞白血病SRC：SCid/NOD小鼠体内增殖的人造血干细胞，SCid造血重建细胞SS：Sezary syndrome，Sezary综合征Stem cell：干细胞STNI：subtotal nodal irradiation，次全淋巴结照射Stomatitis：口炎Subclavian catheter：锁骨下导管Supernatant：上清Syn－BMT：Syngeneic bone marrow transplant：同基因骨髓移植Syngeneic：同基因的TAM：tumor associated macrophage，肿瘤相关巨噬细胞t-AML：treatment associated AML，治疗相关的急性髓性白血病TA－GVHD：transfusion associated graft-versus-host disease，输血相关的移植物抗宿主病TAA：tumor associated antigen，肿瘤相关抗原TBGP：total blood granulocyte pool，总血液粒细胞池TBI：total body irradiation，全身照射Tc：time of cell cycle, 细胞周期时间TCD：T cell depletion, T细胞去除TCL：T cell leukemia/lymphoma，T细胞白血病/淋巴瘤TCR：T cell receptor，T细胞受体TCS：tumor cell survival，肿瘤细胞成活TEN：total enteral nutrition，完全胃肠内营养TF：tissue factor，组织因子TF：thymic factor，胸腺因子TFPI：tissue factor pathway inhibitor，组织因子途径抑制物TGF：therapeutic gain factor，治疗获得系数TGF－β：transforming growth factor-β，转化生长因子βThrombocyte：血小板Thrombocytopenia:血小板减少症TIL：tumor infiltrate lymphocyte,肿瘤浸润淋巴细胞TL：testis leukemia睾丸白血病TLI：total Lymphoid irradiation，全淋巴照射Thrombotic microangiopathy (TMA)：血栓性微血管病TNF：tumor necrosis factor，肿瘤坏死因子TNI：total nodal irradiation，全淋巴结照射TOPO II：topoisomerase II，拓扑易构酶IIToxin：毒素Tpdt：potential doubling time，倍增时间T－PLL：T-prolymphocytic leukemia，T幼淋细胞白血病TPN：total parenteral nutrition，全肠道外营养，静脉高营养TPO：thrombopoietin，促血小板生成素TPS：treatment planning system，治疗计划系统Translocation：易位Trauma：创伤TRM：transplantation related mortality，移植相关死亡率TSC：timed-sequential chemotherapy，时相序贯化疗TSPA：triophosphoramide，噻替派TTP：thrombotic thrombocytopenic purpura，血栓性血小板减少性紫癜Tumor：肿瘤Tumor burden：肿瘤负荷UCB：umbilical cord blood，脐带血Ultrasound：超声Umbilical cord：脐带VAHS：viral associated hemophagocytic syndrome，病毒相关嗜血细胞综合征VGPR：very good partial remission，非常良好的部分缓解Viability：活性Virus：病毒VOD：veno-occlusive disease，静脉阻塞性疾病v-onc: virus oncogene，病毒癌基因VPF: vascular permeability factor，血管渗透因子VZV：varicella zoster virus，水痘带状疱疹病毒WBC：white blood cell，白细胞Whole blood：全血WT：Wilms tumor，肾母细胞瘤Xerostomia：口腔干燥症。
关于干细胞与免疫细胞的临床应用的英语
干细胞与免疫细胞的临床应用1. IntroductionThe clinical application of stem cells and immune cells has been a topic of great interest and debate in the medical field. In recent years, there has been a growing body of research and development in the use of these cells for various medical conditions. In this article, we will explore the potential and challenges of using stem cells and immune cells in clinical settings.2. Understanding Stem CellsFirst, let's delve into the concept of stem cells. Stem cells are undifferentiated cells that have the ability to differentiate into specialized cell types. They are the foundation of development in multicellular organisms, and have the potential to repair, replace, or restore damaged tissues in the body. The use of stem cells in regenerative medicine has shown promise in treating a wide range of diseases and injuries.3. Clinical Applications of Stem CellsStem cell therapy has been studied and applied in various medical fields, including cardiology, neurology, orthopedics,and oncology. For example, in cardiology, stem cells have been used to regenerate cardiac tissue in patients with heart disease. In neurology, stem cell therapy offers potential treatments for conditions such as Parkinson's disease and spinal cord injuries. While there have been significant advancements in the clinical use of stem cells, challenges such as ethical considerations, safety, and regulation still need to be addressed.4. Exploring Immune CellsOn the other hand, immune cells play a critical role in the body's defense against infections and diseases. Different types of immune cells, such as T cells, B cells, and natural killer cells, have unique functions in the immune system. Harnessing the power of immune cells in clinical applications has the potential to revolutionize the treatment of cancer, infectious diseases, and autoimmune disorders.5. Immunotherapy and Cancer TreatmentOne of the most exciting developments in the field of immune cell therapy is the use of immunotherapy in cancer treatment. Immunotherapies, such as chimeric antigen receptor (CAR) T-cell therapy, have demonstrated remarkable success in treating certain types of cancer. By reprogramming a patient's ownimmune cells to recognize and attack cancer cells, immunotherapy offers a targeted and personalized approach to cancer treatment.6. Clinical Challenges and OpportunitiesDespite the significant progress in the clinical applications of stem cells and immune cells, there are still challenges that need to be ovee. These include the need for standardized protocols, long-term safety and efficacy data, and ethical considerations. Additionally, the high cost and accessibility of these treatments pose barriers to widespread implementation. However, with continued research and technological advancements, the potential for stem cell and immune cell therapy to transform medicine is undeniable.7. ConclusionIn conclusion, the clinical application of stem cells and immune cells holds immense potential for advancing the field of medicine. From regenerative medicine to cancer immunotherapy, these novel approaches have the power to revolutionize the way we treat and manage diseases. However, it is vital to approach this field with caution, ensuring that ethical, safety, and regulatory considerations are thoroughlyaddressed. As we continue to uncover the therapeutic capabilities of stem cells and immune cells, the future of medicine looks brighter than ever.8. Personal PerspectivePersonally, I find the intersection of stem cell and immune cell therapy to be a fascinating and promising area of research. The potential to harness the body's own healing mechanisms and immune defenses for clinical applications is a testament to the incredible potential of modern medicine. As we navigate theplexities of translating these scientific advancements into tangible treatments, I am hopeful that the collaboration between researchers, clinicians, and regulatory bodies will ultimately benefit patients in need of innovative therapies.。
免疫细胞学英语
IntroductionImmunocytology, a specialized branch of cellular biology, delves into the intricate world of immune cells, their structure, function, and interactions within the complex network of the immune system. These cells, often referred to as leukocytes or white blood cells, play a pivotal role in defending our bodies against a myriad of pathogens, foreign substances, and even aberrant cells that arise from within. This essay provides a comprehensive, high-quality analysis of immunocytology, examining various aspects of immune cells, including their classification, development, activation mechanisms, effector functions, and the emerging therapeutic applications that harness their power.Classification and Development of Immune CellsThe immune system is composed of a diverse array of cell types, each with distinct roles and characteristics. Broadly, immune cells can be classified into two main categories: innate immune cells and adaptive immune cells. Innate immune cells, such as neutrophils, monocytes/macrophages, dendritic cells (DCs), natural killer (NK) cells, and mast cells, provide the first line of defense against invading pathogens. They recognize conserved pathogen-associated molecular patterns (PAMPs) via pattern recognition receptors (PRRs) and respond rapidly but non-specifically.In contrast, adaptive immune cells, comprising B cells and T cells, offer a highly specific, long-lasting defense. B cells produce antibodies, while T cells execute cytotoxic or helper functions depending on their subsets (CD4+ T helper cells, CD8+ cytotoxic T cells, regulatory T cells, etc.). The development of these immune cells occurs primarily in the bone marrow (for B cells and myeloid cells) and the thymus (for T cells). A tightly regulated process involving hematopoietic stem cell (HSC) differentiation, gene rearrangements, positive and negative selection, and maturation ensures the generation of a diverse and self-tolerant immune repertoire.Activation Mechanisms and Signal TransductionThe activation of immune cells is a finely orchestrated process triggeredby the recognition of antigens or danger signals. For innate immune cells, PRR engagement initiates signaling cascades involving adaptor proteins like MyD88 and TRIF, leading to the activation of transcription factors such as NF-κB and IRF3/7, which drive the expression of pro-inflammatory cytokines, chemokines, and antimicrobial peptides.Adaptive immune cells, particularly T and B cells, require antigen recognition through their unique antigen receptors (TCR for T cells, BCR for B cells). This interaction, when accompanied by appropriate co-stimulatory signals, activates intracellular signaling pathways involving kinases such as Lck, Zap70, and PI3K, ultimately leading to the activation of transcription factors like NF-κB, AP-1, and NFAT. These transcription factors orchestrate the expression of genes involved in cell proliferation, differentiation, and effector function.Effector Functions of Immune CellsInnate immune cells execute various effector functions to combat infections. Neutrophils phagocytose and kill pathogens through the release of reactive oxygen species (ROS) and granule contents. Monocytes/macrophages display similar phagocytic abilities and also present antigens to T cells, produce inflammatory cytokines, and participate in tissue repair. DCs are professional antigen-presenting cells (APCs) that capture, process, and present antigens to naïve T cells, initiating adaptive immune responses. NK cells directly eliminate virus-infected or transformed cells without prior sensitization, relying on the balance of activating and inhibitory receptors interacting with cell surface ligands.Adaptive immune cells contribute to immunity through antibody production and cell-mediated responses. B cells differentiate into plasma cells that secrete antibodies, which neutralize pathogens, opsonize them for enhanced phagocytosis, or activate complement. T cells, upon activation, differentiate into effector subsets: CD4+ T helper cells (Th1, Th2, Th17, Tfh, etc.) that provide help to other immune cells, and CD8+ cytotoxic T cells that directlykill infected or transformed cells. Regulatory T cells (Tregs) maintain immune homeostasis by suppressing excessive immune responses and preventing autoimmunity.Emerging Therapeutic ApplicationsRecent advances in immunocytology have paved the way for innovative therapeutic strategies targeting immune cells. Cancer immunotherapy, for instance, has revolutionized cancer treatment, with approaches such as immune checkpoint inhibitors (e.g., anti-PD-1, anti-CTLA-4 antibodies) that unleash the cytotoxic potential of T cells suppressed by tumor microenvironment. Chimeric antigen receptor (CAR)-T cell therapy involves engineering patient's T cells to express CARs, enabling targeted recognition and destruction of tumor cells. Additionally, adoptive transfer of ex vivo expanded or genetically modified NK cells is being explored for cancer therapy due to their inherent ability to recognize and kill malignant cells.In autoimmune diseases and transplant rejection, therapies targeting immune cells aim to suppress pathogenic immune responses. These include the use of monoclonal antibodies against pro-inflammatory cytokines or their receptors, T cell-depleting agents, and Treg-based therapies. Moreover, modulation of innate immune cells, particularly DCs, through targeted delivery of antigens or immunomodulatory molecules, holds promise for the induction of tolerance in autoimmune and allergic disorders.ConclusionImmunocytology offers a rich tapestry of knowledge, elucidating the complexities of immune cells and their integral role in maintaining host defense. From the classification and development of these cells to the intricate mechanisms governing their activation and effector functions, understanding immunocytology is crucial for both fundamental biological insights and translational applications. The ongoing advancements in this field continue to fuel the development of novel therapeutic strategies that harness the power of immune cells, transforming the landscape of modern medicine in the fight againstinfectious diseases, cancer, and autoimmune disorders.。
Circuit-specific_gene_therapy_is_knocking_on_the_d
Circuit-specific gene therapy is knocking on the door of Parkinson’s diseaseParkinson’s disease (PD) is a prevalent neurodegenerative disorder that affects millions of individuals worldwide.Symptoms of PD typically manifest as movement impairments,including bradykinesia, rigidity, tremors, and postural instability, as well as non-motor symptoms, such as cognitive decline, pain, and depression (Bloem et al., 2021). The fundamental neuropathological hallmarks of PD include the degeneration of dopaminergic neurons in the substantia nigra (SN) and the aggregation of α-synuclein in intracellular inclusions. At present, the primary interventions for PD treatment are levodopa, dopamine agonists, deep brain stimulation (DBS), and physical therapy. However, levodopa administration can lead to intractable side effects such as dyskinesia (Wang & Shih, 2023) and DBS poses risks of long-term psychiatric complications, including chronic depression and personality alterations, as well as infection related to the intracranial electrodes (Volkmann et al., 2010). Consequently,there exists an urgent need for the innovation of targeted and efficacious treatments for PD.Chen et al. (2023) recently documented the development and verification of a novel gene therapy for PD, which successfully reversed the core motor symptoms of PD in both mouse and monkey models (Figure 1). Their research specifically targeted D1 medium spiny neurons (D1-MSNs) in the striatum, which project to the globus pallidus internal segment (GPi) and substantia nigra pars reticulata (SNr), thus forming a direct pathway. D2 medium spiny neurons (D2-MSNs), another important neuronal type in the striatum,project indirectly to the SNr via the globus pallidus external segment (GPe)/subthalamic nucleus (STN), thus forming an indirect pathway. Activation of the direct pathway (comparable to an “accelerator”) facilitates movement, whereas activation of the indirect pathway (comparable to a “brake”) inhibits movement. In PD, degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc) weakens dopaminergic modulation of both D1-MSNs and D2-MSNs. As a result, the direct pathway is repressed while the indirect pathway is enhanced, causing an imbalance between the “accelerator” and “brake”, resulting in motor deficits.Therefore, the study aimed to up-regulate the activity of D1-MSNs associated with the direct pathway and thereby restore movement control equilibrium in PD (Chen et al., 2023).To achieve this objective, a method to precisely manipulatespecific cell types within D1-MSNs is required. Thus, the authors utilized cell type-specific expression by employing a tailored retrograde adeno-associated virus (AAV) with a unique promoter to drive elevated gene expression in D1-MSNs, the only major cell type in the striatum projecting to the SNr. Specifically, the team first engineered several AAV capsid mutants, with the AAV8 mutant, AAV8R, showing improved retrograde infection of D1-MSNs. Subsequent modifications led to the identification of AAV8R12 as the most efficient mutant for labeling D1-MSNs. Next, the authors analyzed a gene expression database and screened for promoters. Through extensive in vivo experimentation, the authors ascertained that the G88 promoter family drove the highest level of gene expression in MSNs. Consequently, by integrating the G88P3/G88P7 promoter with the AAV8R12vector, they obtained a robust manipulation tool capable of labeling D1-MSNs with strong specificity in primates.Next, to modulate the functions of the labeled D1-MSNs, the authors expressed Designer Receptors Exclusively Activated by Designer Drugs (DREADD) effector rM3Ds into D1-MSNs by unilaterally injecting the viral vector AAV8R12-G88P7-rM3Ds -2A -EYFP into the SNr of monkeys. Following the administration of clozapine N-oxide (CNO) and deschloroclozapine (DCZ), ligands that bind with rM3Ds to enable neuronal excitation (Roth, 2016), the monkeys showed marked increases in contraversive rotations, thus demonstrating the efficiency of the toolkit in direct pathway activation.Finally, the same approach was applied to MPP +-treated monkeys, which exhibited PD-like symptoms, including tremor,bradykinesia, and rigidity. Following a single surgical procedure to inject the virus into the SNr, the monkeys receiving regular CNO/DCZ treatments showed rapid recovery and restored motor ability, including increased spontaneous movement, reduced tremor, and improved motor skills.Continuous monitoring of these subjects confirmed the long-term safety of the treatment. Notably, when compared to the standard therapeutic dose of levodopa, the most widely used treatment for PD, this circuit-specific gene therapy not only showed a more rapid reversal of symptoms but also no inducement of observable side effects.Chen et al. (2023) not only established a proof-of-concept for circuit-specific therapeutics, but also effectively leveraged a non-human primate (NHP) model to fully showcase theReceived: 07 November 2023; Accepted: 15 November 2023; Online: 17November 2023Foundation items: This work was supported by the National Natural Science Foundation of China (32160204), Major Science and Technology Projects of Hainan Province (ZDKJ2021032), and STI 2030—Major Projects (2022ZD0208602)This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (/licenses/by-nc/4.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium,provided the original work is properly cited.Copyright ©2023 Editorial Office of Zoological Research, Kunming Institute of Zoology, Chinese Academy of SciencesWang et al. Zool. Res. 2023, 44(6): 1152−1153https:///10.24272/j.issn.2095-8137.2023.353effectiveness and safety of the therapy in PD monkeys. Given the natural occurrence of parkinsonian conditions in monkeys (Li et al., 2021a, 2021b), indicating shared mechanisms and pathologies of PD between NHPs and humans, this approach holds promise for successful clinical translation and application. In contrast, numerous proposed therapeutics have claimed efficacy in alleviating PD symptoms in mice. However, the significant physiological differences between mice and humans, coupled with the fact that mice do not naturally develop PD, have resulted in the failure of many of these mouse-based trials in the end. In this context, Chen et al. (2023) have laid a new foundation for translating cutting-edge biotechnology into feasible pre-clinical practice. Furthermore, recent reports have highlighted various new therapeutic approaches for PD, with several advancing to stages of clinical trial validation. For example, Bayer recently announced positive Phase-I results for its stem cell-based therapy bemdaneprocel (BRT-DA01) for PD, encouraging progression to the next phase of clinical testing. Concurrently, several companies have been developing immunotherapies targeting α-synuclein. Among these, prasinezumab (PRX002), developed by Prothena and Roche, did not achieve the expected outcomes in its Phase-II trials. Nevertheless, PRX002 demonstrated potential signs of disease progression mitigation, such that the companies have resolved to continue a Phase-IIb trial to further validate its efficacy. The ongoing development of novel therapies underscores the complexity of translating basic findings into clinical practice, often presenting more challenges than expected.Given the success of primate PD models, circuit-specific gene therapy shows a promising future in clinical application. Although AAV-mediated therapies are considered safe and sustainable over a long period of time (Kang et al., 2023), challenges remain in terms of potential immune reactions and unknown long-term effects of chemogenetic manipulation. The cost of medication is another concern for stem cell therapies (Chen & Niu, 2019) and immunotherapies. Currently, available immunotherapies (for other diseases) are expensive, hindering expansion of the market. Regarding the therapy proposed by Chen et al. (2023), the market price is uncertain, but it is hoped that it will be affordable for all patients. Although many factors need to be considered before potential clinical trials, we are enthusiastic about the progress made by the team and hope that their therapy opens the door for a new era in PD PETING INTERESTSThe authors declare that they have no competing interests.AUTHORS’ CONTRIBUTIONSY.Q.W., M.Y., and Z.S.G. conceived and wrote the draft. Y.Q.W. generated the figure. All authors read and approved the final version of the manuscript.Yue-Qi Wang1,2,3, Ming Yin1,2,*, Zhe-Shan Guo1,2,*1 State Key Laboratory of Digital Medical Engineering, School ofBiomedical Engineering, Hainan University, Haikou, Hainan570228, China2 Key Laboratory of Biomedical Engineering of Hainan Province, One Health Institute, Hainan University, Haikou, Hainan 570228,China3 Shenzhen Technological Research Center for PrimateTranslational Medicine, Shenzhen-Hong Kong Institute of Brain Science, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong 518055 China *Corresponding authors, E-mail: ********************.cn;**********************.cnREFERENCESBloem BR, Okun MS, Klein C. 2021. Parkinson's disease. The Lancet, 397(10291): 2284−2303.Chen YF, Hong ZX, Wang JY, et al. 2023. Circuit-specific gene therapy reverses core symptoms in a primate Parkinson’s disease model. Cell,doi: 10.1016/j.cell.2023.10.004.Chen ZZ, Niu YY. 2019. Stem cell therapy for Parkinson's disease using non-human primate models. Zoological Research, 40(5): 349−357.Kang L, Jin SL, Wang JY, et al. 2023. AAV vectors applied to the treatment of CNS disorders: clinical status and challenges. Journal of Controlled Release, 355: 458−473.Li H, Su LY, Yang LX, et al. 2021a. A cynomolgus monkey with naturally occurring Parkinson's disease. National Science Review, 8(3): nwaa292.Li H, Yao YG, Hu XT. 2021b. Biological implications and limitations of a cynomolgus monkey with naturally occurring Parkinson's disease. Zoological Research, 42(2): 138−140.Roth BL. 2016. DREADDs for neuroscientists. Neuron, 89(4): 683−694. Volkmann J, Daniels C, Witt K. 2010. Neuropsychiatric effects of subthalamic neurostimulation in Parkinson disease. Nature Reviews Neurology, 6(9): 487−498.Wang R, Shih LC. 2023. Parkinson's disease - current treatment. Current Opinion in Neurology, 36(4): 302−308.Figure 1 Circuit-specific gene therapy opens the door for a new era of Parkinson’s disease (PD) therapeuticsZoological Research 44(6): 1152−1153, 2023 1153。
免疫力下降的英语
IntroductionThe human immune system is an intricate network of biological processes and structures designed to protect the body against a multitude of pathogens, including viruses, bacteria, fungi, parasites, and even abnormal cells. It operates through a sophisticated balance of innate and adaptive responses, ensuring that invading threats are recognized, neutralized, and eliminated efficiently. However, this robust defense mechanism can sometimes falter, leading to a decline in immunity. This extensive analysis delves into the multifaceted nature of declining immunity, exploring various factors that contribute to its occurrence, the consequences it brings, and potential strategies for prevention and management.I. Factors Contributing to Declining ImmunityA. Age-Related ImmunosenescenceOne of the most significant factors influencing immune function is age. Immunosenescence, the gradual deterioration of the immune system with advancing age, is characterized by a decline in the production and function of immune cells, particularly T and B lymphocytes. This leads to reduced responsiveness to new antigens, decreased vaccine efficacy, and increased susceptibility to infections, autoimmune disorders, and cancer.B. Chronic StressProlonged exposure to stressors, whether physical, emotional, or psychological, can have detrimental effects on immune function. Chronic stress triggers the release of stress hormones like cortisol, which can suppress the immune response by inhibiting the production of cytokines and other immune mediators. This can result in impaired immune cell proliferation, reduced antibody synthesis, and weakened pathogen clearance capacity.C. Malnutrition and Nutrient DeficienciesA balanced diet rich in essential nutrients is vital for maintaining optimal immune function. Deficiencies in key vitamins (e.g., A, C, D, E, B6, B12), minerals (e.g., zinc, selenium, iron), and omega-3 fatty acids can impair immune cell development, maturation, and activity. Additionally, obesity and excessive caloric intake can lead to chronic low-grade inflammation, further compromising immune function.D. Sleep Deprivation and DisruptionSleep plays a critical role in immune regulation, as it is during this restorative state that immune cells undergo proliferation, differentiation, and activation. Chronic sleep deprivation or disruption can dysregulate immune responses, increasing susceptibility to infections and exacerbating inflammatory conditions.E. Sedentary Lifestyle and Lack of ExerciseRegular physical activity has immunomodulatory effects, enhancing the circulation of immune cells, improving their functional capacity, and reducing systemic inflammation. Conversely, a sedentary lifestyle can lead to immune dysfunction, increasing the risk of infections and chronic diseases.F. Environmental FactorsExposure to environmental pollutants, such as air pollution, heavy metals, and pesticides, can induce oxidative stress and inflammation, impairing immune function. Moreover, tobacco smoke contains numerous toxic substances that can directly damage immune cells and disrupt their signaling pathways.G. Medications and Medical ConditionsCertain medications, such as immunosuppressive drugs used in organ transplantation or chemotherapy, can significantly dampen immune function. Additionally, medical conditions like HIV/AIDS, autoimmune diseases, and chronic infections can also cause immune decline.II. Consequences of Declining ImmunityA. Increased Susceptibility to InfectionsA weakened immune system is less effective at recognizing and eliminating pathogens, rendering individuals more vulnerable to infections. This can manifest as recurrent or prolonged infections, increased severity of illness, and slower recovery times.B. Impaired Response to VaccinesDeclining immunity can compromise the body's ability to mount a robust and long-lasting immune response following vaccination, reducing vaccine effectiveness and leaving individuals susceptible to vaccine-preventable diseases.C. Exacerbation of Chronic DiseasesDiminished immune function can contribute to the development and progression of chronic inflammatory conditions, such as cardiovascular disease, diabetes, and neurodegenerative disorders, by promoting inflammation and impairing tissue repair processes.D. Increased Risk of CancerA compromised immune system may be less efficient at detecting and eliminating precancerous or malignant cells, potentially leading to the development or progression of various types of cancer.III. Strategies for Prevention and Management of Declining ImmunityA. Lifestyle Modifications1. Healthy Eating: Ensuring a balanced diet rich in essential nutrients, antioxidants, and anti-inflammatory foods can support immune function.2. Regular Exercise: Engaging in moderate-intensity physical activity most days of the week can enhance immune cell function and reduce inflammation.3. Quality Sleep: Prioritizing adequate sleep duration and maintaining good sleep hygiene can help maintain immune homeostasis.4. Stress Management: Incorporating stress-reducing techniques like mindfulness meditation, yoga, or cognitive-behavioral therapy can help mitigate the negative impact of stress on the immune system.B. Immunization and Preventive Healthcare1. Timely Vaccinations: Adhering to recommended vaccination schedules can help prevent infections and boost immune defenses against specific pathogens.2. Regular Health Check-ups: Regular screenings and early detection of chronic diseases can facilitate timely intervention and help preserve immune function.C. Targeted Interventions for Specific Risk Factors1. Treating Nutrient Deficiencies: Supplementation or dietary modification to address specific nutrient deficiencies can support immune health.2. Managing Chronic Conditions: Effective management of underlying medical conditions, such as diabetes or autoimmune disorders, can help preserve immune function.3. Reducing Exposure to Environmental Toxins: Adopting measures to minimize exposure to environmental pollutants can help protect immune health.D. Advanced Therapies and Research1. Immunomodulatory Drugs: Investigating and developing novel immunotherapies or repurposing existing drugs to enhance or restore immune function in individuals with compromised immunity.2. Precision Medicine: Utilizing genomics, proteomics, and other advanced technologies to tailor preventive and therapeutic interventions based on individual immune profiles.ConclusionDeclining immunity is a complex phenomenon influenced by a myriad of factors, ranging from intrinsic processes like aging to modifiable lifestyle choices and environmental exposures. Its consequences can be far-reaching, affecting an individual's susceptibility to infections, response to vaccines, and risk of chronic diseases. By understanding these factors and implementing targeted prevention and management strategies, we can work towards preserving and enhancing immune function across the lifespan, ultimately contributing to improved overall health and wellbeing.。
DiO (细胞膜绿色荧光探针) 说明书
DiO (细胞膜绿色荧光探针)产品编号 产品名称包装 C1038DiO (细胞膜绿色荧光探针)10mg产品简介：DiO 即DiOC18(3)，全称为3,3′-dioctadecyloxacarbocyanine perchlorate ，是最常用的细胞膜荧光探针之一，呈现绿色荧光。
DiO 是一种亲脂性膜染料，进入细胞膜后可以侧向扩散逐渐使整个细胞的细胞膜被染色。
DiO 在进入细胞膜之前荧光非常弱，仅当进入到细胞膜后才可以被激发出很强的荧光。
DiO 被激发后可以发出绿色的荧光，DiO 和磷酯双层膜结合后的激发光谱和发射光谱参考下图。
其中，最大激发波长为484nm ，最大发射波长为501nm 。
DiO 的分子式为C 53H 85ClN 2O 6，分子量为881.72，CAS number 为34215-57-1。
DiO 可以溶解于无水乙醇、DMSO 和DMF ，其中在DMSO 溶解度大于为10mg/ml 。
发现较难溶解时可以适当加热，并用超声处理以促进溶解。
DiO 被广泛用于正向或逆向的，活的或固定的神经等细胞或组织的示踪剂或长期示踪剂(long-term tracer)。
DiO 通常不会明显影响细胞的生存力(viability)。
DiO 对于细胞膜染色的荧光强度通常要低于DiI ，有时对于某些经过固定的组织的染色效果欠佳。
DiO 除了最简单的细胞膜荧光标记外，还可以用于检测细胞的融合和粘附，检测发育或移植过程中细胞迁移，通过FRAP(Fluorescence Recovery After Photobleaching)检测脂在细胞膜上的扩散，检测细胞毒性和标记脂蛋白等。
用于细胞膜荧光标记时，DiO 的常用浓度为1-30μM ，最常用的浓度为5-10μM 。
DiO 可以直接染色活的细胞或组织，染色时间通常为5-20分钟。
对于固定的细胞或组织，通常宜使用配制在PBS 中的4%多聚甲醛进行固定，使用其它不适当的固定液会导致荧光背景较高。
一种癌症治疗方法英文
一种癌症治疗方法英文IntroductionCancer is a complex disease that affects millions of people worldwide. Conventional cancer treatments, such as surgery, chemotherapy, and radiation therapy, have been the mainstay of cancer management for decades. However, these treatments often come with significant side effects and are not always effective in eradicating cancer cells. In recent years, a new cancer treatment method has emerged, offering hope for better outcomes and reduced side effects. This article aims to introduce this innovative approach and explore its potential benefits. Immunotherapy: The BasicsImmunotherapy, also known as biologic therapy, is a form of cancer treatment that uses the body's own immune system to fight cancer cells. The immune system is a complex network of cells, tissues, and organs that work together to defend the body against harmful pathogens and abnormal cells. Immunotherapy harnesses the power of the immune system and stimulates it to identify and kill cancer cells more effectively. Types of ImmunotherapyThere are several types of immunotherapy currently being developed and used in cancer treatment. These include:Checkpoint InhibitorsCheckpoint inhibitors are drugs that block certain proteins on immunecells or cancer cells, allowing the immune system to recognize and attack cancer cells more effectively. These drugs have shown promising results in treating various types of cancer, including melanoma, lung cancer, and kidney cancer.CAR-T Cell TherapyCAR-T (Chimeric Antigen Receptor T-cell) therapy involves modifying a patient's own T cells, a type of immune cell, to express a receptor that recognizes cancer cells. Once infused back into the patient's body, these modified T cells can seek out and destroy cancer cells. CAR-T cell therapy has shown remarkable success in treating certain types of blood cancers, such as leukemia and lymphoma.Cancer VaccinesCancer vaccines are designed to stimulate the immune system to recognize and attack cancer cells. These vaccines can be made from cancer cells or specific proteins found on cancer cells. When administered, they trigger an immune response against cancer cells. Cancer vaccines have the potential to prevent cancer recurrence and improve treatment outcomes.Monoclonal AntibodiesMonoclonal antibodies are laboratory-produced proteins that can target specific molecules on cancer cells. By attaching to these molecules, monoclonal antibodies can either directly kill cancer cells or stimulatethe immune system to destroy them. Monoclonal antibody therapy has proven effective in treating breast cancer, lymphoma, and colorectal cancer.Benefits of ImmunotherapyImmunotherapy offers several advantages over conventional cancer treatments:Reduced Side EffectsUnlike chemotherapy and radiation therapy, which often damage healthy cells along with cancerous ones, immunotherapy specifically targets cancer cells, minimizing potential side effects. This targeted approach results in fewer severe adverse effects, such as hair loss, nausea, and weakened immune system.Long-lasting EffectsImmunotherapy has shown the ability to create long-lasting effects, even after treatment is completed. The immune system's memory allows it to recognize and attack cancer cells that may reappear in the future. This immunological memory offers the potential for long-term remission and improved survival rates.Improved Quality of LifeDue to the reduced side effects and long-lasting effects, patients undergoing immunotherapy tend to experience an improved quality of life compared to those treated with traditional methods. The ability tocarry out daily activities without significant physical and emotional distress is a significant benefit for cancer patients.ConclusionImmunotherapy represents a promising and rapidly advancing field of cancer treatment. Its ability to harness the body's immune system and target cancer cells specifically has led to improved treatment outcomes and reduced side effects. As researchers continue to explore and refine immunotherapy techniques, there is hope that this innovative approach will become a standard of care for a wider range of cancer types.。
当科学家英语作文发明癌症的药
当科学家英语作文发明癌症的药Cancer: A Treacherous Foe, a Glimmer of Hope.For centuries, the scourge of cancer has plagued humanity, leaving an unfathomable trail of suffering and loss. Its relentless assault on human lives has spurred a relentless quest for a cure, a remedy to vanquish this formidable adversary.The advent of modern medicine has unveiled a plethoraof breakthroughs, offering new hope in the battle against cancer. Surgery, chemotherapy, radiation therapy, and immunotherapy have become formidable weapons in the fight against this insidious disease. Yet, despite these advances, cancer remains a formidable foe, its enigmatic nature constantly outwitting our best efforts.Undeterred, scientists across the globe continue to delve into the depths of cancer research, seeking tounravel its intricate complexities and pave the way for acure. Amid this tireless pursuit, a glimmer of hope has emerged—the potential to harness the power of our own bodies to combat cancer.The Promise of Immunotherapy.Immunotherapy, a groundbreaking approach to cancer treatment, empowers the body's natural defenses to recognize and eliminate cancer cells. Unlike traditional therapies that directly target cancer, immunotherapy stimulates the immune system, transforming it into a potent ally in the fight against disease.One of the most promising avenues in immunotherapy is the use of checkpoint inhibitors, drugs that unleash the immune system's ability to attack cancer cells. These inhibitors work by blocking molecules that serve as brakes on the immune response, allowing T cells, the body's primary defense against cancer, to recognize and attack cancer cells with renewed vigor.Targeted Therapies: Precision Strikes Against Cancer.Another significant breakthrough in cancer treatment is the development of targeted therapies, drugs that disrupt specific genetic mutations or proteins that drive cancer growth. By honing in on these molecular vulnerabilities, targeted therapies offer a more precise and effective approach to combating cancer.Examples of targeted therapies include imatinib, which targets a specific mutation in chronic myeloid leukemia, and trastuzumab, which targets a protein overexpressed in HER2-positive breast cancer. These therapies have revolutionized the treatment of these cancers,significantly improving patient outcomes and offering new hope for a cure.Harnessing Nature's Arsenal.The pursuit of a cancer cure has also led scientists to explore the medicinal potential of plants and other natural sources. Traditional medicines have been used for centuries to treat a wide range of ailments, and modern research isuncovering the scientific basis behind their effectiveness.Curcumin, a compound found in turmeric, has been shownto exhibit potent anti-cancer properties. It has been found to inhibit cancer cell growth, promote apoptosis (cell death), and suppress angiogenesis (the formation of new blood vessels that supply cancer cells).Another promising natural compound is resveratrol,found in red wine and grapes. Resveratrol has been shown to activate sirtuins, a family of proteins involved inlongevity and cancer suppression. It has also been found to inhibit cancer cell growth and metastasis.Challenges and Opportunities.Despite the remarkable progress made in cancer research, significant challenges remain. Cancer is a highly complex and heterogeneous disease, and no single treatment approach is effective against all types of cancer. Additionally, cancer cells can develop resistance to treatments over time, making it imperative to continually develop new therapies.However, these challenges also present opportunitiesfor innovation and discovery. By deepening our understanding of cancer biology and exploring novel treatment strategies, scientists are charting a path towards a future where cancer is no longer a death sentence but a manageable disease.Collaboration and Innovation: Fueling Progress.The quest for a cancer cure is a global endeavor that requires collaboration and resource sharing among scientists, clinicians, and pharmaceutical companies. Open access to data, funding for research, and international partnerships are essential to accelerate the pace of discovery and innovation.Through multidisciplinary approaches, researchers are harnessing the power of genomics, computational biology, and artificial intelligence to develop more effective personalized therapies. By leveraging these cutting-edge technologies, scientists are charting new frontiers incancer treatment, offering patients tailored solutionsbased on their individual genetic makeup and tumor characteristics.The Future of Cancer Treatment: Promise and Possibility.The future of cancer treatment holds tremendous promise, with advancements in immunotherapy, targeted therapies, and natural therapies offering new avenues for hope. While the path ahead may be fraught with challenges, the unwavering dedication of scientists, clinicians, and advocates is fueling progress towards a world where cancer is a diseaseof the past.As we continue to unlock the secrets of cancer and develop innovative treatments, we inch closer to the day when this formidable foe is conquered, leaving behind a legacy of hope and triumph. The battle against cancer isfar from over, but the unwavering spirit of discovery andthe collective determination to conquer this disease will ultimately prevail.。
211216928_嵌合抗原受体Ｔ_细胞治疗原发性肝癌临床研究进展
ＤＯＩ：１０．３９６９／ｊ．ｉｓｓｎ．１００１－５２５６．２０２３．０５．００４嵌合抗原受体Ｔ细胞治疗原发性肝癌临床研究进展李 爽１，２，刘哲睿１，２，赵 琦３，陆荫英２１北京大学三 二临床医学院，北京１０００３９；２解放军总医院第五医学中心肝病医学部，北京１０００３９；３澳门大学健康科学院，澳门特别行政区９９９０７８通信作者：陆荫英，ｌｕｙｉｎｙｉｎｇ１９７３＠１６３．ｃｏｍ（ＯＲＣＩＤ：００００－０００２－７７３７－２３３４）摘要：原发性肝癌具有起病隐匿以及早期诊断困难等特点，治疗手段有限且效果不佳。
嵌合抗原受体（ＣＡＲ）Ｔ细胞疗法是经基因编辑修饰的Ｔ淋巴细胞识别肿瘤特异性抗原并活化Ｔ淋巴细胞，发挥肿瘤杀伤作用。
ＣＡＲ－Ｔ细胞疗法治疗血液肿瘤取得重大进展，近年来在实体瘤领域也有了很好的临床疗效，尽管ＣＡＲ－Ｔ细胞治疗技术已经从第一代发展到第五代，但在实体瘤领域仍存在诸多挑战。
本文将对ＣＡＲ－Ｔ细胞治疗原发性肝癌的机制以及相关研究进展进行全面的综述，包括目前ＣＡＲ－Ｔ细胞疗法治疗原发性肝癌主要的靶点ＧＰＣ３、ＡＦＰ、ＭＵＣ１、ＮＫＧ２Ｄ等，ＣＡＲ－Ｔ细胞治疗与溶瘤病毒，逐渐兴起的免疫检查点抑制剂等联合治疗，以及对以上靶点以及治疗方式的生物学研究、临床前研究和临床研究的回顾，并对ＣＡＲ－Ｔ细胞治疗原发性肝癌面临的挑战及解决措施进行汇总。
为未来ＣＡＲ－Ｔ细胞疗法在肝癌领域的临床发展提供参考。
关键词：嵌合抗原受体；Ｔ淋巴细胞；癌，肝细胞；治疗学基金项目：深圳市科技创新委员会可持续发展专项（ＫＣＸＦＺ２０２００２０１１００６４４８）ＣｌｉｎｉｃａｌｒｅｓｅａｒｃｈａｄｖａｎｃｅｓｉｎｃｈｉｍｅｒｉｃａｎｔｉｇｅｎｒｅｃｅｐｔｏｒＴ－ｃｅｌｌｔｈｅｒａｐｙｆｏｒｐｒｉｍａｒｙｌｉｖｅｒｃａｎｃｅｒＬＩＳｈｕａｎｇ１，２，ＬＩＵＺｈｅｒｕｉ１，２，ＺＨＡＯＱｉ３，ＬＵＹｉｎｙｉｎｇ２．（１．ＰｅｋｉｎｇＵｎｉｖｅｒｓｉｔｙ３０２ＣｌｉｎｉｃａｌＭｅｄｉｃａｌＳｃｈｏｏｌ，Ｂｅｉｊｉｎｇ１０００３９，Ｃｈｉｎａ；２．ＤｅｐａｒｔｍｅｎｔｏｆＬｉｖｅｒＤｉｓｅａｓｅｓ，ＴｈｅＦｉｆｔｈＭｅｄｉｃａｌＣｅｎｔｅｒｏｆＣｈｉｎｅｓｅＰＬＡＧｅｎｅｒａｌＨｏｓｐｉｔａｌ，Ｂｅｉｊｉｎｇ１０００３９，Ｃｈｉｎａ；３．ＦａｃｕｌｔｙｏｆＨｅａｌｔｈＳｃｉｅｎｃｅｓ，ＵｎｉｖｅｒｓｉｔｙｏｆＭａｃａｕ，ＭａｃａｏＳｐｅｃｉａｌＡｄｍｉｎｉｓｔｒａｔｉｖｅＲｅｇｉｏｎ９９９０７８，Ｃｈｉｎａ）Ｃｏｒｒｅｓｐｏｎｄｉｎｇａｕｔｈｏｒ：ＬＵＹｉｎｙｉｎｇ，ＬＵＹｉｎｙｉｎｇ１９７３＠１６３．ｃｏｍ（ＯＲＣＩＤ：００００－０００２－７７３７－２３３４）Ａｂｓｔｒａｃｔ：Ｐｒｉｍａｒｙｌｉｖｅｒｃａｎｃｅｒ（ＰＬＣ）ｈａｓｔｈｅｆｅａｔｕｒｅｓｏｆｉｎｓｉｄｉｏｕｓｏｎｓｅｔａｎｄｄｉｆｆｉｃｕｌｔｉｅｓｉｎｅａｒｌｙｄｉａｇｎｏｓｉｓ，ｗｉｔｈｌｉｍｉｔｅｄａｎｄｉｎｅｆｆｅｃｔｉｖｅｔｈｅｒａｐｅｕｔｉｃｏｐｔｉｏｎｓ．Ｃｈｉｍｅｒｉｃａｎｔｉｇｅｎｒｅｃｅｐｔｏｒ（ＣＡＲ）Ｔ－ｃｅｌｌｔｈｅｒａｐｙｉｓａｇｅｎｅｔｉｃａｌｌｙｍｏｄｉｆｉｅｄＴ－ｃｅｌｌｔｈｅｒａｐｙｔｈａｔｒｅｃｏｇｎｉｚｅｓｔｕｍｏｒ－ｓｐｅｃｉｆｉｃａｎｔｉｇｅｎｓａｎｄａｃｔｉｖａｔｅｓＴｃｅｌｌｓｔｏｅｘｅｒｔａｔｕｍｏｒ－ｋｉｌｌｉｎｇｅｆｆｅｃｔ．ＣＡＲＴ－ｃｅｌｌｔｈｅｒａｐｙｈａｓｍａｄｅｇｒｅａｔｐｒｏｇｒｅｓｓｉｎｔｈｅｔｒｅａｔｍｅｎｔｏｆｈｅｍａｔｏｌｏｇｉｃａｌｔｕｍｏｒｓａｎｄｈａｓａｃｈｉｅｖｅｄａｇｏｏｄｃｌｉｎｉｃａｌｅｆｆｅｃｔｉｎｔｈｅｆｉｅｌｄｏｆｓｏｌｉｄｔｕｍｏｒｓｉｎｒｅｃｅｎｔｙｅａｒｓ，ａｎｄａｌｔｈｏｕｇｈＣＡＲＴ－ｃｅｌｌｔｈｅｒａｐｙｈａｓｄｅｖｅｌｏｐｅｄｆｒｏｍｔｈｅｆｉｒｓｔｔｏｔｈｅｆｉｆｔｈｇｅｎｅｒａｔｉｏｎ，ｔｈｅｒｅａｒｅｓｔｉｌｌｍａｎｙｃｈａｌｌｅｎｇｅｓｉｎｔｈｅｆｉｅｌｄｏｆｓｏｌｉｄｔｕｍｏｒｓ．ＴｈｉｓａｒｔｉｃｌｅｃｏｍｐｒｅｈｅｎｓｉｖｅｌｙｒｅｖｉｅｗｓｔｈｅｍｅｃｈａｎｉｓｍｓｏｆＣＡＲＴ－ｃｅｌｌｔｈｅｒａｐｙｆｏｒＰＬＣａｎｄｒｅｌａｔｅｄｒｅｓｅａｒｃｈａｄｖａｎｃｅｓ，ｉｎｃｌｕｄｉｎｇｔｈｅｍａｉｎｔａｒｇｅｔｓｓｕｃｈａｓＧＰＣ３，ＡＦＰ，ＭＵＣ１，ａｎｄＮＫＧ２ＤｉｎＣＡＲＴ－ｃｅｌｌｔｈｅｒａｐｙｆｏｒＰＬＣ，ＣＡＲＴ－ｃｅｌｌｔｈｅｒａｐｙｆｏｒＰＬＣａｎｄｏｎｃｏｌｙｔｉｃｖｉｒｕｓ，ａｎｄｃｏｍｂｉｎｅｄｔｒｅａｔｍｅｎｔｗｉｔｈｉｍｍｕｎｅｃｈｅｃｋｐｏｉｎｔｉｎｈｉｂｉｔｏｒｓ，ａｓｗｅｌｌａｓｔｈｅａｄｖａｎｃｅｓｉｎｔｈｅｂｉｏｌｏｇｉｃａｌ，ｐｒｅｃｌｉｎｉｃａｌ，ａｎｄｃｌｉｎｉｃａｌｓｔｕｄｉｅｓｏｎｔｈｅｓｅｔａｒｇｅｔｓａｎｄｔｒｅａｔｍｅｎｔｍｏｄａｌｉｔｉｅｓａｎｄｔｈｅｃｈａｌｌｅｎｇｅｓａｎｄｓｏｌｕｔｉｏｎｓｆｏｒＣＡＲＴ－ｃｅｌｌｔｈｅｒａｐｙｉｎｔｈｅｔｒｅａｔｍｅｎｔｏｆＰＬＣ，ｓｏａｓｔｏｐｒｏｖｉｄｅａｒｅｆｅｒｅｎｃｅｆｏｒｔｈｅｆｕｔｕｒｅｃｌｉｎｉｃａｌｄｅｖｅｌｏｐｍｅｎｔｏｆＣＡＲＴ－ｃｅｌｌｔｈｅｒａｐｙｉｎｌｉｖｅｒｃａｎｃｅｒ．Ｋｅｙｗｏｒｄｓ：Ｒｅｃｅｐｔｏｒｓ，ＣｈｉｍｅｒｉｃＡｎｔｉｇｅｎ；Ｔ－Ｌｙｍｐｈｏｃｙｔｅｓ；Ｃａｒｃｉｎｏｍａ，Ｈｅｐａｔｏｃｅｌｌｕｌａｒ；ＴｈｅｒａｐｅｕｔｉｃｓＲｅｓｅａｒｃｈｆｕｎｄｉｎｇ：ＴｈｅＳｃｉｅｎｃｅＴｅｃｈｎｏｌｏｇｙａｎｄＩｎｎｏｖａｔｉｏｎＣｏｍｍｉｓｓｉｏｎｏｆＳｈｅｎｚｈｅｎＭｕｎｉｃｉｐａｌｉｔｙ（ＫＣＸＦＺ２０２００２０１１００６４４８）９１０１李爽，等．嵌合抗原受体Ｔ细胞治疗原发性肝癌临床研究进展 原发性肝癌是中国乃至全世界较为常见的恶性肿瘤，发病率居于世界第七（４．７％），死亡率位于全世界第三（８．３％）［１］，由于原发性肝癌起病隐匿且早期诊断困难，大多数患者确诊时已经是中晚期，常规治疗手段有限，患者５年生存率较差［１］。
免疫细胞治疗药物临床试验的风险管理
免疫细胞治疗药物临床试验的风险管理作者：赵真李刚徐瑛来源：《上海医药》2021年第13期摘要免疫细胞疗法作为目前最先进的疗法之一，在癌症等疾病的治疗中起着重要作用。
免疫细胞治疗药物由于在原料来源和制备工艺等方面与传统药物差异很大，临床试验阶段存在诸多不确定因素和风险。
本文通过梳理国内外相关指导原则，结合我国临床试验实施现况，就免疫细胞治疗药物临床试验的风险管理作一探讨，供业界借鉴和参考。
关键词免疫细胞治疗药物临床试验风险管理中图分类号：R951 文献标志码：C 文章编号：1006-1533（2021）13-0010-04Risk management of clinical trials of immune cell therapy drugsZHAO Zhen， LI Gang， XU Ying（Shanghai Center for Drug Evaluation and Inspection， Shanghai 201203， China）ABSTRACT As one of the most advanced therapies， immune cell therapy plays an important role in the treatment of cancer and other diseases. There are many uncertain factors and risks in the clinical trials of immune cell therapy drugs， which are due to their great differences from traditional medicinal products in terms of cell source and manufacturing process. We review the relevant guidelines， investigate the current situation of clinical trial implementation in China， and discuss the risk management of clinical trials of immunotherapy so as to provide reference for its clinical use.KEy WORDS immune cell therapy drugs； clinical trials； risk management2017年，免疫细胞治疗药物tisagenlecleucel（商品名：Kymriah）和axicabtagene ciloleucel （商品名：Yescarta）先后獲得美国FDA批准，引起医药学界的广泛关注。
传染病护理学重点(Key points of infectious diseases nursing)
传染病护理学重点（Key points of infectious diseases nursing）2. pathogenicity of pathogens during infection:(1) invasiveness: the ability of pathogens to invade the organism and spread in vivo. Such as: invasive ability, soluble tissue capacity, penetration and so on.(2): including virulence exotoxin, endotoxin and virulence factors.(3) quantity: the same pathogen, the number of invasion is often proportional to its pathogenic ability; in different infectious diseases, the minimum number of pathogens causing an infectious disease varies greatly.(4) variation3. the immune response during infection: nonspecific immunity and specific immunity(1) nonspecific immunity: the organism is a scavenging mechanism for foreign bodies entering the body. It is obtained by heredity, without antigen specificity, or congenital immunity.Three main natural barriers - skin, blood, cerebrospinal fluid, placenta, phagocytosis, humoral factors. Phagocytosis: mononuclear phagocyte system has nonspecific phagocytosis.Humoral factors: including fluid infusion, lysozyme and various cytokines, such as interleukin, tumor necrosis factor,interferon gamma, etc..(2) specific immunity: the specific immune response produced against the original antigen by the original recognition is acquired by an active immunity. Humoral immunity mediated by B lymphocytes and cell-mediated immunity by T lymphocytes are included.7. the route of transmission of viral hepatitis(1) fecal oral transmission: the main route of transmission of hepatitis A and e.;(2) the spread of blood and body fluids: mainly spread hepatitis B, hepatitis C, d way(3) mother to child transmission: mainly through the placenta, birth canal, childbirth, breast-feeding and feeding. It is also an important route of transmission of HBV infection.8. detection of hepatitis viruses (markers)The hepatitis A: Anti -HAV-IgG serum: recent infection index, is a marker for diagnosis of hepatitis A in the main. Serum anti HAV-IgG: protective antibody can be seen in patients who have been inoculated with hepatitis A vaccine or who have been infected with HAV. HAV RNAThe hepatitis b:Surface antigen (HBsAg) and surface antibody (anti -HBs): HBsAgpositive in HBV infected persons, HBV infection 3 weeks after the first occurrence of HBsAg. Anti -HBs positivity is seen mainly in patients who have been vaccinated against hepatitis B vaccine or who have been infected with HBV and who have developed immunity.E antigen (HBeAg) and e antibody (anti -HBe): HBeAg only appeared in HBsAg positive serum, HBeAg positive indicated that HBV replication was active and infectivity was stronger; anti -HBe appeared after HBeAg disappeared.Core antigen (HBcAg) and its antibody (anti -HBc): HBcAg mainly exists in the nucleus of infected liver. Anti -HBc occurs in the 3~5 week after HBsAg. Type IgM anti -HBc exists in acute or chronic hepatitis B with acute exacerbation. Type IgG anti -HBc is a marker of past infection.Hepatitis B virus DNA (HBV) and DNAP are the most direct, specific and sensitive indicators of HBV infection. Both positive suggest the existence and replication of HBV, infectivity is strong.The hepatitis c:Hepatitis C virus RNA (HCV, RNA);Hepatitis C virus antibodies (anti -HCV): a marker for HCV infection, not a protective antibody.The HDAg and HDV RNA: hepatitis DThe hepatitis E: Anti -HEV-IgM and anti -HEV-IgG9. antiviral drugs for chronic hepatitis:1) interferon: indications for the use of chronic hepatitis: (HBV) in active replication; hepatitis is in active phase.Interferons are generally used in 10~65 year old patients with severe heart and kidney dysfunction and decompensated cirrhosis.2) nucleoside drugs: HBV, DNA replication has a strong inhibitory effect, there is no obvious adverse reactions.Lamivudine was first used in clinic. Other: adefovir, entecavir.3) Chinese herbal medicine: Shandougen agents such as Ganyanlin injection etc..[viral hepatitis] commonly used nursing diagnosis / measuresThe activity intolerance and impaired liver function and energy metabolism disorders.Rest and activities: acute hepatitis, chronic hepatitis, active stage, severe hepatitis should be in bed rest, liver function is normal, 1~3 months later can resume daily activities and work, but should avoid excessive exertion and heavy physical labor.The life care: serious illness need to assist patients for dining, bathing, toilet and other life care.Psychological counseling.The nutritional disorders: less than body requirements and loss of appetite, vomiting, diarrhea, digestion and absorption dysfunction.1) introduce the importance of a reasonable diet;2) eating principle:Acute hepatitis: should eat light, easy to digest, rich in vitamin fluids; can be prescribed, intravenous supplement of glucose, fat milk and vitamins.Jaundice subsided period: gradually increase diet, eat less and more meals, avoid overeating. Diet principle for chronic patients: energy intake in bed rest or rest should be 84 to 105kJ/ (kg, d). Moderate activity (work) should be 126 to 147kJ/ (kg, D). The protein of 1.5 ~ 2.0g/ (kg? D), with high quality protein, such as milk, lean pork, fish and other carbohydrates; 300 ~ 400g/d; fat tolerance limit of about 50 ~ 60g/d, with vegetable oil; eat more fruits, vegetables and other foods rich in vitamin.Hepatitis cirrhosis and severe hepatitis: light and low saltIV diet of various types of hepatitis patients: should not be long-term intake of high sugar and high calorie diet, abdominaldistension can reduce the production of gas products (milk, soy products) intake. All types of hepatitis patients should be prohibited from drinking alcohol.3) observe the gastrointestinal symptoms: To observe the appetite, nausea, vomiting, acid and other symptoms.4) assess the patient's nutritional status: measure your weight every week and assess your daily intake.The potential complications of bleeding1) observe the condition of the patient: observe the bleeding position, development and regression of the patient.2) general nursing: rest and diet guidance; encourage patients to eat high protein, high vitamin, digestible diet or semi liquid, fast and excellent, too rough food; maintain defecate unobstructed.Bleeding and nursing of common site:3) skin bleeding: to avoid artificial injury or lead to increased bleeding; high fever patients disable alcohol bath cooling.4) nasal bleeding: first, prevent the nasal mucosa dry and bleeding, keep the relative humidity in the room about 50% to 60%;Avoid artificial induced bleeding: do not force the nose;A small amount of bleeding can be filled with cotton or gelatin sponge. When bleeding is serious, the nasal cavity is filled with Vaseline gauze.5), oral gingival bleeding: with a soft toothbrush, do not usea toothpick, avoid eating fried, prickly, food containing bone, shelled nuts, eating slowly.The potential complications of adverse reactions: interferon treatment1) pre medication instruction;2) nursing during the medication - common adverse reactions and treatment:Fever: general injection of interferon in the first 3~5 times, ranging from low fever to high fever, may be accompanied by headache, muscle, bone pain, fatigue, weakness and so on. Patients should be instructed to drink more water, stay in bed, and treat them as necessary;Gastrointestinal reactions: nausea, vomiting, anorexia, diarrhea and so on. Generally symptomatic treatment, severe withdrawal.Alopecia: after withdrawal, can be restored.Liver function impairment: jaundice, increased ALT, etc.. Continue treatment or withdrawal as appropriate.Neuropsychiatric symptoms: depression, anxiety, etc. Severe cases should be reduced or discontinued.The change of peripheral blood white blood cell count decreased more common, if the white blood cells in more than 3 * 109/L should adhere to treatment, the doctor's advice to give leukogenic drugs; if the white cell is less than 3 * 109/L or neutrophil <1.5 * 109/L, <40 * 109/L or platelets can reduce the dose of interferon and withdrawal.3) periodic reviewMain points of treatment for epidemic encephalitis b:The symptomatic treatment:1) high fever: to physical cooling mainly, sustained high fever with repeated convulsions, can be Ya Dong sleep therapy, chlorpromazine and promethazine each 0.5 ~ 1mg/d intramuscular injection.2) convulsions or convulsions: treatment measures include the removal of the cause of the disease and the onset of convulsion (preferably diazepam (diazepam)) in the town.3) according to the cause of respiratory failure: given the therapy of brain edema caused by dehydrating agent treatment; central respiratory failure by respiratory stimulant, such as lobeline (Toban) and Nikethamide; respiratory tract obstruction, attention suctioning, postural drainage,inhalation of phlegm drugs; also can use vasodilator agents such as anisodamine and scopolamine.4) increased intracranial pressure: early adequate dehydration treatment, commonly used 20% mannitol or sorbitol, furosemide, glucocorticoid.The Chinese medicine treatment: White Tiger Decoction, qingwenbaidu drink etc.. The medicine can be used as an Niuhuang Niuhuang pill.The recovery and sequelae of treatment: pay attention to functional training, including language, swallowing and limb function, physical therapy, acupuncture, physical therapy, feasible hyperbaric oxygen therapy.。
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[Specific immune cell therapy against ovarian cancer in
vivo and in vitro].
Ai Zheng. 2008; 27(12):1244-50 (ISSN: 1000-467X)
Chang XH; Cheng HY; Cheng YX; Ye X; Guo HF; Fu TY; Zhang L; Zhang G; Cui H
Gynecologic Oncology Center, Peking University People's Hospital, Beijing, 100044, P. R. China.
BACKGROUND & OBJECTIVE: 6B11minibody (6B11mini), an anti-idiotypic vaccine against human ovarian cancer, has been proven to induce specific humoral and cellular immunity against ovarian cancer in vivo and in vitro. This study was to investigate the safety and efficacy of using 6B11mini as an antigen to treat ovarian cancer.
METHODS: After being loaded with purified 6B11mini, dendritic cells (DCs) were co-cultured with peripheral blood mononucleocytes (PBMNC) and stimulated by various cytokines, including CD3 monoclonal
antibody,interleukin-2, interferon-gamma, to obtain
6B11mini-ovarian-cytokine-induced-killer cells (6B11-O-CIK).
Tumor-forming ability was determined using soft agar colony-forming assay in vitro and nude mice xenografts in vivo. The acute toxicity of 6B11-OCIK at different doses was observed in BALB/c mice. Cytotoxicity of 6B11-OCIK to different target cells was detected using 51Cr release test in vitro. The ovarian tumor model was established using severe combined immune deficiency (SCID) mice transplanted with human ovarian cancer cell line SKOV3. The tumor growth was detected after injection of 6B11-OCIK into SCID mice. Injection of CIK, PBMNC and physiological saline were used as controls.
RESULTS: After a cultural period of 14 days in soft agar, SKOV3 cell clones were well formed with a ratio of 50%; while 6B11-OCIK, CIK and PBMNC did not form any clones. All nude mice injected with human cervical carcinoma cell line HeLa (positive control) grew tumors after 14 days, and mice injected with 6B11-OCIK, CIK, PBMNC and normal human fetal lung fibroblast WI-38 cells did not form tumors after 13 weeks. BALB/c mice did not show any abnormal response half an hour after the administration of 6B11-OCIK cells at different doses. Mice were sacrificed 13 days after treatments, but no distinct abnormality of the main organs were found. 6B11-OCIK exerted specific cytotoxicity against tumor cells with positive OC166-9, which was related to the limitation of MHC. The tumor weights of SCID mice transplanted with SKOV3 cells were significantly lighter in 6B11-OCIK treatment group than in the saline group(P=0.023); while the tumor weights
were not significantly different between the 6B11-OCIK group with CIK and the PBMNC group(P=0.540; P=0.285).
CONCLUSIONS: The application of 6B11-OCIK in vivo has reached the safety standard. 6B11-OCIK has the inhibitory effect on the growth of ovarian cancer cells.。