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Hypersensitive Reactions

1. Type I

Hypersensitivity

2. Type II Hypersensitivity 3. Type III Hypersensitivity 4. Type IV Hypersensitivity

1. Basic concepts
Hypersensitivity reactions are harmful antigen-specific immune
responses , occur when an individual who has been primed by an innocuous antigen subsequently encounters the same antigen , produce tissue injury and dysfuntion.

Allergen the antigens that give rise to immediate hypersensitivity Atopy
the genetic predisposition to synthesize inappropriate levels of IgE

specific for external allergens

Types of hypersensitivity

I II III IV

2. Type I hypersensitivity
1) 2) 3) 4) 5) Characteristics Components and cells The process and mechanism Commen diseases of type I Hypersensitivity Therapy for type I Hypersensitivity

1) Characteristics Occur and resolve quickly Mediated by serum IgE Systemic and regional tissue dysfuntion Genetic predisposition .

2) Components and cells in Type I hypersensitivity Allergen pollen dust mite insects etc selectively activate CD4+Th2 cells and B cells Allergin IgE IgE and its production mainly produced by mucosal B cells in the lamina prapria special affinity to the same cell IL-4 is essential to switch B cells to IgE production High affinity receptor of the IgE on mast cell and basophil Eosinophil .

DC.High affinity receptor of the IgE on mast cell and basophil FcIRI (high affinity ) FcIR FcIRII (low affinity ) (CD23) on circulating basophil. T. basophil Lysis sCD23(IgE-BF) Switch B cell to IgE production . connective tissue mast cell FcIRIIa FcIRIIb on B cell on B. M .

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3 The process and mechanism of Type I hypersensitivity 1) Priming stage 2) Activating stage Crosslinkage Enzyme reaction Degranulation of mast cell . basophil last more than half a year 3) Effect stage Immediate/early phase response: Mediated by histamine Start within seconds Last several hours Late-phase response Mediated by new-synthesized lipid mediators Take up 8-12hours to develop Last several days .

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Mechanism of type I hypersensitivity Primary Generation Allergen Secondary Individual IgE Adhesion IgE binds to the FcIRI on mast cell and basophil Allergen binds to the IgE on primed target cell Crosslikage of FcIRI Degranulate and release the biological mediators Preformed granule mediators Histamine Bradykinin New generated mediators Leukotrienes PAF Prostaglandin D2 Dilate capillaries. increase mucus secretion. contract smooth muscle Systemic anaphylaxis Skin Respiratory tract Degist tract .increase permeability.

release and synthesis of biological mediators of primed target cells .Allergen Hydroxyl phosphalipid Phosphatidylcholine Phosphalipid Phosphoration of ITAM Arachidonic acid MAPK Activation of PTK Inactivated PKC Activated PKC AcetylCOX transferases Myosin LOX Endoplasmic reticulum Phosphoration of Light chain Lipid mediatiors Cell membrane Degranulation Histamine Degranulation .

Histamine: Dilate blood vessel Increase vascular permeability 2. Platelet activating factor (PAF) : Agglutinate and activate platelets to release histamine 5. Prostaglandin: High concentration of PGE low concentration of PGE Inhibit the secretion of histamine promote the release of histamine 4. Bradykinin : Vasodilator function ECF-A : . Leukotrienes: Bronchial smooth muscles contract Asthmas 3. Eosinophil chemotactic factor 6.The biological mediator on effect stage 1.

4. Skin allergy: . Common disease of type I hypersensitivity 1. Systemic anaphylaxis: a very dangerous syndrome 1) Anaphylactic drug allergy 2) Anaphylactic serum allergy penicillin 2. Respiratory allergic diseases : 1) Allergic asthma 2) Allergic rhinitis acute response. Gastrointestinal allergic diseases : The lack of SIgA protein hydrolase Undigested protein Allergen 4. chronic response 3.

inhibit mast cell degranulation 2) Mediator antagonism Chlor-Trimeton Antihistamine Acetylsalicylic acid Bradykinin antagonism 3) Improve the responsibility of target organs 4. Drug therapy 1) Stabilization of triggering cells sodium cromoglycate stabilize the membrane. Therapy of type I hypersensitivity 1. Temporality Blocking antibody 3.5. Allergen avoidance : Atopy patch test 2. Desensitivity therapy / Hyposensitization : 1) Allogenic serum desensitivity therapy: Repeated injection small amounts of allergen. New immunotherapy . 2) Specific allergen desensitivity therapy IgG+allergen Neutralizing antibody.

Type II Hypersensitivity 1. Characteristic features 2.3. Mechanism of Type II Hypersensitivity 3. Common diseases of Type II Hypersensitivity .

1. Characteristic features Primed IgG or IgM + Antigen or hapten on membrane Injury and dysfunction of target cells .

Opsonic phagocytosis Combined opsonic activities D. ADCC of NK C. Effect of complement Cell injury ways of type II hypersensitivity .Allergen Stimulate Antibody Cell A.

Drug antigen. changed or modified self tissue cells Antigen : Blood group antigen.2. Surface antigen on target cells Target cells: Normal tissue cell. Antibody. Mechanism of Type II hypersentivity 1. Common antigen. Self-antigen modified by physical factors or infection Antigen-antibody complex 2. complement and modified self-cell Activate complement Opsonic phogacytosis MJ NK T Lyse target cells Destroy target cells ADCC Promote /surpress the target cell funcion Stimulating or blocking effect .

phagocyte Stimulate / block Lyse target cell Destroy target cell ADCC Target cell injury Change the function ofTarget cell Mechanism of Type II hypersensitivity . IgM) Activate complement Opsonic phagocytosis NK .Antigen or hapten on cell Antibody (IgG.

: first baby Rh+(Ab). Foreign antigen or hapten Penicillin Quinin Pyramidone RBC Platlet hemolytic anemia thrombocytopenic purpura Granulocyte agranulocytosis ii.3. second baby Rh+. Self-antigen Drug conversion from a hapten to a full antigen induce self antibody autoimmune hemolytic anemia . fetal RBC destroyed 3) Autoimmune hemolytic anemia and type II drug reaction i. severely destroy RBC nonhemolysis : repeat transfusion of allogenic HLA drug anaphylactic shock penicilline 2) Hemolytic disease of newborn Mother Rh. Common disease of type II hypersensitivity 1)Transfusion reaction hemolysis : mismatch of ABO blood group.

Anti -glomerular basement membrane nephritis -Hemolytic streptococcus and human glomerular basement membrane ---cross reaction Common antigen ---nephrotoxic nephritis 5.Hyperthyroidism or hypothyroidism²receptor diseases .4. Super acute rejection in allogenic organ transplantation 6. Goodpasture syndrome 7.

Common disease of type III hepersensitivity . Characteristics 2. Mechanism of type III hepersensitivity 3.4. type III hypersensitivity 1.

1 characteristics Larger immune complex Free Ag + Primed Ab Deposit in tissue or blood vessel wall Inflammation .

2 Mechanism of type III hypersensitivity Formation of the intermediate immune complex Deposition of the intermediate immune complex Tissue injury by the immune complex .

Soluble antigen Body Antibody Immune complex Small molecular soluble Immune complex intermediate molecular soluble Immune complex Large molecular insoluble Immune complex Deposit on the basement of capillaries Combine and activate complement system Basophils and mast cells C3a.C5a.C3b Infiltration of neutrophils Release of vasoactive amine Eliminate by phogacytosis Platelets Blood Clotting Mechanisms Release of vasoactive amine Phagocytose complex Aggregation of platlets Thrombus Bleeding Increase vascular permeability Edema Increase vascular permeability Release the enzymes in lysosome Edema Tissue injury Local or systemic immune complex diseases .

3. Ulcer Human local reaction: insulin-dependent diabetes mellitus (IDDM) 2. arthritis. Chronic immune complex disease SLE Rheumatoid arthritis RF+IgG Deposit on synovial membrane . Local immune complex disease Arthus reaction Experimental local reaction.fever. common disease of type III hypersensitivity 1. skin rash Streptococcus infection Acute immune complex glomerulonephritis : 3. Acute systemic immune complex disease serum sickness Anti-serum Ab+Ag Pinicillin Sulfanilamide systemic tissue injury . Necrotic vasculitis vasculitis.

5. Type IV hypersensitivity 1 2 3 characteristics of type IV hepersensitivity mechanism of type IV hepersensitivity common diseases of type IV hepersensitivity .

Inflammatory response .1. Characteristics Interaction of primed T cells and associated antigen Infiltration of Mononuclear Cells.

Mechanism of type IV hypersensitivity Formation of effector and memory T cells Inflammation and cytotoxicity caused by effector T cells 1) Inflammation and tissue injury mediated by CD4+Th1 Release chemokines and cytokines Immune injury mainly caused by infiltration of mononuclear cells and lymphocytes 2) Cytotoxicity of CD8+CTL .2.

CD8+) CD4+ T cell Release Secondary contact Primed T cell Cytokines IL-2 TNF-F INF-K TF MCF MIF MAF SRF Infiltration of monocyte and MJ Proliferation of T cell Exudation and edema Cytotoxicity CD8+ T cell Directly kill target cells Inflammation characterized by infiltration of MJ .Antigen Induce T cell (CD4+. And tissue injury Mechanism of type IV hypersensitivity . monocyte.

multiple immune injury . papula. several types of hypersensitivity . water blister.3. drug red rash.hypersensitivity involved Same drug (penicillin). dermatitis 3) Acute rejection of allogenic transplantation and immune response in local tumor mass Same disease (SLE). Common disease of type IV hypersensitivity 1) Infectious delayed type hypersensitivity OT( Old Tuberculin ) test 2) Contact dermatitis : Paint.

‡ Master the processes and mechanisms of type I-IV hypersensitivity ‡ Familiar with therapy of type I hypersensitivity ‡ Comprehend common diseases of type I-IV hypersensitivity .