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Hypersenns III,IV

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    Type III Hypersensitivity

    Immune Complex Mediated Reaction

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    Type III: Immune Complex Mediated Reaction

    *When antibodies (Ig G or Ig M) and antigen coexistimmune complexes are formed

    *Immune complexes are removed by reticuloendoth. syst.

    *Some immune complexesescape phagocytosis

    *Immune complexes deposited in tissues on the basementmembrane of blood vessels and cause tissue injury

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    Mechanism Of Tissue Injury

    Immune complexes trigger inflammatory processes:

    activate release

    1) Immune complexes the complement anaphylatoxins C3a, C5a

    stimulate release

    degranulation of basophiles and mast cells histamine

    Histamine vascular permeability and help deposition of immune complexes

    2) Neutrophils are attracted to the site by immune complexes and releaselysosomal 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

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    Clinical conditions of Type III Hypersensitivity

    Diseases produced by immune complexes are those inwhich 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

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    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

    vasculitis

    leading to microthrombi formation

    vascular occlusion

    necrosis

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    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

    feverurticaria

    * 10 days after injection arthralgia

    lymphadenopathy

    splenomegalyglomerulonephritis

    antidiphtheritic serum

    e.g. treatment with penicillinsul honamides

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    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 repeatedinhalation of dust , mould spores

    5- Endogenous antigen antibody complexes involved inautoimmune diseases

    e.g. SLE, rheumatoid arthritis

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    Type IV

    Cell MediatedDelayed Type Hypersensitivity

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    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- and TNF)

    attract lymphocytes

    * Cytokines activate macrophages

    induce inflammation

    * Tissue damage results from products of activated macrophages

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    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, Freis test in

    lymphogranuloma venereum

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    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 o

    macrophages which give rise to epitheloidal and giantcell granuloma

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    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, formimmunogenic substances

    * DTH reaction to these immunogenic subst. lead to:

    eczyma

    inflammtory reaction of skin in rash

    vesicular eruption

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    Type IV Hypersensitivity Clinical Conditions

    4) Autoimmune diseases and graft rejection are due toin part to delayed hypersensitivity reactions

    5) Insulin dependant diabetes mellitus

    T-cells invade the pancreatic islets and specificallydestroy insulin secreting beta cells

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    Thanks


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2. (iii) (ii) (ii) (iv) (iii) 8?0r) 3118 (iii) (iv) v) vi ...2. (iii) (ii) (ii) (iv) (iii) 8?0r) 3118 (iii) (iv) v) vi) vii) viii) Ox) (x) (Xll) 3Trq 3Tl-q arg, -à t?

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