病理学-免疫性疾病
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(From Robbins Basic Pathology ,2003）
Tissue reactions: variable in severity
Mildest may be only edema; Serioust may be stoke or death (drug/serum allergy);
Immune system: A Two-edged sword
Dependence on intact immunity; The culprit behind the immune-mediated injury.
Section 1 Hypersensitivity Reactions
1. Type I hypersensitivity
② Rabies vaccine may rise to encephalitis
systemic lupus erythematosus
SLE is an autoimmune, multisystem disease of various manifestations and variable behavior.
③ Hidden antigens exposure
(3) Cross-reactions (molecular mimicry)
① Antibodies to streptococcal antigens may react with constituents of cardiac muscle or connective tissue in rheumatic fever.
Reaction is triggered by mast cells, basophils;
IgE also direct damage by recruiting inflammatory cells, many are eosinophils.
2. Type II Hypersensitivity
Antireceptor antibodies disturb the normal function of receptors. In this example, antibodies against acetylcholine receptor impair neuromuscular
transmission in myasthenia gravis. (From Robbins Basic Pathology ,2003）
Slide 7.10
来自百度文库
② Antibody-dependent cell-mediated cytotoxicity (ADCC).
May be relevant to: ➢ Graft rejection ➢ The destruction of targets too large to be
phagocytosed, such as parasites or tumor cells.
Etiology and Pathogenesis
Slide 7.15
(From Robbins Basic Pathology ,2003）
4. Type Ⅳ Hypersensitivity (Cell-
Mediated )
The principal mechanism of response to a variety of microbes.
(Anaphylactic type)
Immediate hypersensitivity reaction, resulting from release of pharmacologically active inflammatory mediators.
Slide 7.9
Activation of mast cells in type I hypersensitivity and release of their mediators. ECF, eosinophil chemotactic factor; NCF, neutrophil chemotactic factor; PAF, platelet-activating factor.
Delayed hypersensitivity in the skin. Immunohistochemistry staining reveals a predominantly perivascular cellular infiltrate that marks positively with anti-CD4 antibodies. ( Dr. Louis Picker) .
Schematic illustration of the three sequential phases in the induction of systemic type Ⅲ (immune complex) hypersensitivity.
(From Robbins Basic Pathology ,2003）
Antibody bound to cell surface antigen causes fixation of complement to cell surface with subsequent lysis via the membrane attack complex.
Cells coated with antibodies and complement C3b fragments render themselves susceptible to phagocytosis.
Under the influence of cytokines, the epitheloid cells fuse to form multinuclear giant cells.
A section of a lymph node shows several granulomas, each made up of an aggregate of epithelioid cells and surrounded by lymphocytes. The granuloma in the center shows several multinucleate giant cells. ( Dr. Trace Worrell)
(From Robbins Basic Pathology ,2003）
Slide 7.17
Section 2 Autoimmune Diseases
1. Definition:
Breakdown of one or more mechanisms of self-tolerance result in an immunologic attack against “ self-antigens”, which leads to the autoimmune diseases.
3. Multiple organs damage.
Skin, kidneys, serosal membrane, joints and heart.
4. Variant Clinical manifestation.
Diagnostic criteria is needed.
5. Recurrence, with 90% and 80% 5 or 10-year survive.
(From Robbins Basic Pathology ,2003）
Slide 7.14
Immune complex vasculitis. The necrotic vessel wall is replaced by smudgy, pink “fibrinoid” (Dr. Trace Worrell)
Cytolytic or cytotoxic reactions
(1) Mechanism:
① Complement-dependent reactions ➢ Transfusion reactions ➢ Autoimmune hemolytic anemia ➢ Certain drug reactions
Slide 7.16
Slide 7.18
The perivascular CD4+ T cell infiltrate is replaced by macrophages over a period of 2-3 weeks.
Upon activation, the accumulated macrophages becomes large, flat and epitheloid.
Slide 7.11
ADCC involves killing cell types that bear Fc receptors for IgG (e.g., NK cells, macrophages). . (From Robbins Basic
Pathology ,2003）
③Antibody-mediated cellular dysfunction Antibodies impair or dysregulate cell function without causing cell injury or imflammation. ➢ Myasthenia gravis: muscle weakness ➢ Graves’ disease: hyperthyroidism
Slide 7.12
3. Type Ⅲ Hypersensitivity (Immune complex-mediated)
Deposition of antibody-antigen complexes;
Complement activation;
Accumulation of polymorphonuclear leukocytes.
Slide 7.13
Schematic representation of the pathogenesis of immune complex-mediated tissue injury. The morphologic consequences are depicted as boxed areas. .
(2) Alteration of self-proteins (modification of the molecule)
① Partial degradation of autoantigens.
② Complexing of self-antigens with drugs or micro-organisms.
2. Mechanism
(1) Breakdown of tolerance ① Bypass of helper T cell tolerance ② Imbalance of suppressor-helper T cell
function ③ Genetic fators ④ Emergence of a sequestered antigen ⑤ Polyclonal lymphocyte activation
SLE- Characteristics
1. A fairly common disease ----1:2500 Predominantly in young women—1:700.( female:male=9:1)
2. Mainly conducted by humoral immunity. autoantibodies: antinuclear antibodies
Type IV hypersensitivity is mediated by specifically sensitized T cells.
(2) Diseases:
① Chronic active hepatitis ② Contact dermatitis ③ Graft rejection ④ Tuberculosis
Tissue reactions: variable in severity
Mildest may be only edema; Serioust may be stoke or death (drug/serum allergy);
Immune system: A Two-edged sword
Dependence on intact immunity; The culprit behind the immune-mediated injury.
Section 1 Hypersensitivity Reactions
1. Type I hypersensitivity
② Rabies vaccine may rise to encephalitis
systemic lupus erythematosus
SLE is an autoimmune, multisystem disease of various manifestations and variable behavior.
③ Hidden antigens exposure
(3) Cross-reactions (molecular mimicry)
① Antibodies to streptococcal antigens may react with constituents of cardiac muscle or connective tissue in rheumatic fever.
Reaction is triggered by mast cells, basophils;
IgE also direct damage by recruiting inflammatory cells, many are eosinophils.
2. Type II Hypersensitivity
Antireceptor antibodies disturb the normal function of receptors. In this example, antibodies against acetylcholine receptor impair neuromuscular
transmission in myasthenia gravis. (From Robbins Basic Pathology ,2003）
Slide 7.10
来自百度文库
② Antibody-dependent cell-mediated cytotoxicity (ADCC).
May be relevant to: ➢ Graft rejection ➢ The destruction of targets too large to be
phagocytosed, such as parasites or tumor cells.
Etiology and Pathogenesis
Slide 7.15
(From Robbins Basic Pathology ,2003）
4. Type Ⅳ Hypersensitivity (Cell-
Mediated )
The principal mechanism of response to a variety of microbes.
(Anaphylactic type)
Immediate hypersensitivity reaction, resulting from release of pharmacologically active inflammatory mediators.
Slide 7.9
Activation of mast cells in type I hypersensitivity and release of their mediators. ECF, eosinophil chemotactic factor; NCF, neutrophil chemotactic factor; PAF, platelet-activating factor.
Delayed hypersensitivity in the skin. Immunohistochemistry staining reveals a predominantly perivascular cellular infiltrate that marks positively with anti-CD4 antibodies. ( Dr. Louis Picker) .
Schematic illustration of the three sequential phases in the induction of systemic type Ⅲ (immune complex) hypersensitivity.
(From Robbins Basic Pathology ,2003）
Antibody bound to cell surface antigen causes fixation of complement to cell surface with subsequent lysis via the membrane attack complex.
Cells coated with antibodies and complement C3b fragments render themselves susceptible to phagocytosis.
Under the influence of cytokines, the epitheloid cells fuse to form multinuclear giant cells.
A section of a lymph node shows several granulomas, each made up of an aggregate of epithelioid cells and surrounded by lymphocytes. The granuloma in the center shows several multinucleate giant cells. ( Dr. Trace Worrell)
(From Robbins Basic Pathology ,2003）
Slide 7.17
Section 2 Autoimmune Diseases
1. Definition:
Breakdown of one or more mechanisms of self-tolerance result in an immunologic attack against “ self-antigens”, which leads to the autoimmune diseases.
3. Multiple organs damage.
Skin, kidneys, serosal membrane, joints and heart.
4. Variant Clinical manifestation.
Diagnostic criteria is needed.
5. Recurrence, with 90% and 80% 5 or 10-year survive.
(From Robbins Basic Pathology ,2003）
Slide 7.14
Immune complex vasculitis. The necrotic vessel wall is replaced by smudgy, pink “fibrinoid” (Dr. Trace Worrell)
Cytolytic or cytotoxic reactions
(1) Mechanism:
① Complement-dependent reactions ➢ Transfusion reactions ➢ Autoimmune hemolytic anemia ➢ Certain drug reactions
Slide 7.16
Slide 7.18
The perivascular CD4+ T cell infiltrate is replaced by macrophages over a period of 2-3 weeks.
Upon activation, the accumulated macrophages becomes large, flat and epitheloid.
Slide 7.11
ADCC involves killing cell types that bear Fc receptors for IgG (e.g., NK cells, macrophages). . (From Robbins Basic
Pathology ,2003）
③Antibody-mediated cellular dysfunction Antibodies impair or dysregulate cell function without causing cell injury or imflammation. ➢ Myasthenia gravis: muscle weakness ➢ Graves’ disease: hyperthyroidism
Slide 7.12
3. Type Ⅲ Hypersensitivity (Immune complex-mediated)
Deposition of antibody-antigen complexes;
Complement activation;
Accumulation of polymorphonuclear leukocytes.
Slide 7.13
Schematic representation of the pathogenesis of immune complex-mediated tissue injury. The morphologic consequences are depicted as boxed areas. .
(2) Alteration of self-proteins (modification of the molecule)
① Partial degradation of autoantigens.
② Complexing of self-antigens with drugs or micro-organisms.
2. Mechanism
(1) Breakdown of tolerance ① Bypass of helper T cell tolerance ② Imbalance of suppressor-helper T cell
function ③ Genetic fators ④ Emergence of a sequestered antigen ⑤ Polyclonal lymphocyte activation
SLE- Characteristics
1. A fairly common disease ----1:2500 Predominantly in young women—1:700.( female:male=9:1)
2. Mainly conducted by humoral immunity. autoantibodies: antinuclear antibodies
Type IV hypersensitivity is mediated by specifically sensitized T cells.
(2) Diseases:
① Chronic active hepatitis ② Contact dermatitis ③ Graft rejection ④ Tuberculosis