Type III Hypersensitivity. Immune Complex Mediated Reaction
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1 Type III Hypersensitivity Immune Complex Mediated Reaction
2 Type III: Immune Complex Mediated Reaction *When antibodies (Ig G or Ig M) and antigen coexist immune complexes are formed *Immune complexes are removed by reticuloendoth. syst. *Some immune complexes escape phagocytosis *Immune complexes deposited in tissues on the basement membrane of blood vessels and cause tissue injury
3 Mechanism Of Tissue Injury Immune complexes trigger inflammatory processes: activate release 1) Immune complexes the complement anaphylatoxins C3a, C5a stimulate degranulation of basophiles and mast cells release histamine Histamine vascular permeability and help deposition of immune complexes 2) Neutrophils are attracted to the site by immune complexes and release lysosomal enzymes which damage tissues and intensify the inflammat. Pro. 3) Platelets are aggregated with two consequences a- release of histamine b- form of microthrombi which lead to ischemia
4 Clinical conditions of Type III Hypersensitivity Diseases produced by immune complexes are those in which antigens persists without being eliminated as: a- Repeated exposure to extrinsic antigen b- injection of large amounts of antigens c- Persistent infections d- Autoimmunity to self components
5 1- Arthus Reaction * This is a local immune complex deposition phenomenon e.g. diabetic patients receiving insulin subcutaneously edema * Local reactions in the form of erythema necrosis deposited * Immune complexes in small blood vessels leading to vasculitis microthrombi formation vascular occlusion necrosis
6 2- Serum Sickness * A systemic immune complex phenomenon * Injection of large doses of foreign serum * Antigen is slowly cleared from circulation * Immune complexes are deposited in various sites fever urticaria * 10 days after injection arthralgia lymphadenopathy splenomegaly glomerulonephritis antidiphtheritic serum e.g. treatment with penicillin
7 Type III Hypersensitivity Clinical Conditions 3- Post-streptococcal glomerulonephritis glomerulitis associated with infective endocarditis 4- Hypersensitive pneumonitis (farmer lung) immune complexes depositition in lung after repeated inhalation of dust, mould spores 5- Endogenous antigen antibody complexes involved in autoimmune diseases e.g. SLE, rheumatoid arthritis
8 Type IV Cell Mediated Delayed Type Hypersensitivity
9 Type IV: Cell Mediated Delayed Type Hypersensitivity triggering DTH reactions by TH1 * T-cells cause tissue injury by or directly killing target cells by CD8 * TH1 and CD8 T cells secrete cytokines (IFN-γ and TNF) attract lymphocytes * Cytokines activate macrophages induce inflammation * Tissue damage results from products of activated macrophages
10 Tuberculin Type Hypersensitivity * When PPD is injected intradermally in sensitized person * Local indurated area appears injection site (48-72 hs) * Indurations due to accumulation Of: macrophages and lymphocytes * Similar reactions observed in diseases e.g. brucellosis, lepromin test in leprosy, Frei s test in lymphogranuloma venereum
11 Granulomatous lesions * In chronic diseases : T.B., Leprosy, schistosomiases * Intracellular organisms resist destruction by macrophag. * Persistent antigen in tissues stimulate local DTH reaction * Continuous release of cytokines leads to accumulation of macrophages which give rise to epitheloidal and giant cell granuloma
12 Contact Dermatitis * Contact of skin with chemical substances or drugs e.g. poison, hair dyes, cosmetics, soaps, neomycin * These substances enter skin in small molecules * They are haptens that attached to body proteins,, form immunogenic substances * DTH reaction to these immunogenic subst. lead to: inflammtory reaction of skin in eczyma rash vesicular eruption
13 Type IV Hypersensitivity Clinical Conditions 4) Auto immune diseases and graft rejection are due to in part to delayed hypersensitivity reactions 5) Insulin dependant diabetes mellitus T-cells invade the pancreatic islets and specifically destroy insulin secreting beta cells
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