Transcript Immunopathology

Section 2 Hypersensitivity
Reactions
1. Type I hypersensitivity
(Anaphylactic type)
Immediate hypersensitivity reaction,
resulting from release of
pharmacologically active mediators.
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.
(From Robbins Basic Pathology
,2003）
Slide 7.9
(2) Tissue reactions: variable in severity
Mildest may be only edema. Reaction
is triggered by mast cells, basophils.
If inflammatory cells are present,
many are eosinophils.
(3) Diseases
① Urticaria and angioneurotic edema
② Asthma
③ Hay fever
④Insect allergy: serious or fatal
anaphylaxis may follow. Edema of
larynx, with airway obstruction may
occur.
2. Type II Hypersensitivity
Cytolytic or cytotoxic reactions
(1) Mechanism:
① Complement-dependent reactions
Transfusion reactions
Erythroblastosis fetal
Autoimmune hemolytic anemia
Certain drug reactions
②Antibody-dependent cell-mediated cytotoxicit
(ADCC).
May be relevant to:
 Graft rejection
 The destruction of targets too large to be
phagocytosed, such as parasites or tumor cells.
③Antibody-mediated cellular dysfunction
 Myasthenia gravis: muscle weakness
 Graves’ disease: hyperthyroidism
Schematic illustration of three different mechanisms of antibody-mediated
injury in type Ⅱ hypersensitivity. A, Complement-dependent reactions that
lead to lysis of cells or render them susceptible to phagocytosis.
(From Robbins Basic Pathology ,2003）
Slide 7.10
Antibody-dependent cell-mediated cytotoxicity (ADCC). IgG-coated target
cells are killed by cells that bear Fc receptors for IgG (e.g., NK cells,
macrophages). . (From Robbins Basic Pathology ,2003）
Slide 7.11
Antireceptor antibodies disturb the normal function of receptors. In this
example, acetylcholine receptor antibodies impair neuromuscular transmission
in myasthenia gravis. (From Robbins Basic Pathology ,2003）
Slide 7.12
3. Type Ⅲ Hypersensitivity
(Immune complex-mediated)
(1) Reaction types
① Arthus reaction
② serum sickness
③ Collagen diseases
(2) Toxic complex diseases:
① Acute glomerulonephritis
② Systemic lupus erythematosus
③ Necrotizing angiitides
④ Rheumatoid arthritis
⑤ Progressive systemic sclerosis
⑥ Dermatomyositis etc.
Schematic illustration of the three sequential phases in the
induction of systemic type Ⅲ (immune complex) hypersensitivity.
(From Robbins Basic Pathology ,2003）
Slide 7.13
Schematic representation of the pathogenesis of immune complex-mediated
tissue injury. The morphologic consequences are depicted as boxed areas. .
(From Robbins Basic Pathology ,2003）
Slide 7.14
Immune complex vasculitis. The necrotic vessel wall is replaced by
smudgy, pink “fibrinoid” (Dr. Trace Worrell)
Slide 7.15
(From Robbins Basic Pathology ,2003）
4. Type Ⅳ Hypersensitivity
(Cell-Mediated )
Delayed hypersensitivity reaction
(1) Tissue reaction: Consist of
parenchymal destruction associated
with perivascular lymphocytic and
macrophage reaction.
(2) Diseases:
① Chronic active hepatitis
② Viral exanthem(皮疹）
③ Contact dermatitis
④ Graft rejection
⑤ Inflammatory bowel disease.
Delayed hypersensitivity in the skin. Immunoperoxidase staining
reveals a predominantly perivascular cellular infiltrate that marks
positively with anti-CD4 antibodies. ( Dr. Louis Picker) .
(From Robbins Basic Pathology ,2003）
Slide 7.16
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
Schematic illustration of
the events that give rise to
the formation of
granuloma in type Ⅳ
hypersensitivity reactions.
Note the role played by T
cell-derived cytokines. .
(From Robbins Basic Pathology
,2003）
Slide 7.18