Hypersensitivity

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Hypersensitivity

  1. 1. HypersensitivityClassificationHypersensitivity reactions are classified into four types:type I, type II, type III (immediate reactions)type IV (delayed reactions)
  2. 2. Type I Hypersensitivity AllergensInhalants: Pollen grains, Fungal allergensInjectants: drugsContact: Antiseptic spray
  3. 3. Type I hypersensitivity is known as immediate or hypersensitivity. The reaction may involve:■ Skin (urticaria and eczema),■ Eyes (conjunctivitis),■ Nasopharynx (rhinorrhea, rhinitis),■ Bronchopulmonary tissues (asthma)■ Gastrointestinal tract (gastroenteritis).
  4. 4. ■ The mechanism of reaction involvesproduction of IgE, in response to certainantigens (allergens).■ IgE has very high affinity for its receptoron mast cells and basophils.■ A subsequent exposure to the same allergencross links the cell-bound IgE and triggersthe release of various active substances.
  5. 5.  Cross-linking of IgE Fc-receptor is important in mast cell triggering. Mast cell degranulation is preceded by increased Ca++ influx, which is a crucial process.
  6. 6. Mediators of Immediate Hypersensitivity Preformed mediators in granules:Hypersensitivity Table 1 Mediators of I bronchoconstriction, mucus secretion, histamine vasodilatation, vascular permeability tryptase proteolysis ECF-A attract eosinophil and neutrophils Newly formed mediators: leukotriene B4 basophil attractant leukotrieneC4, same as histamine ( 1000x more potent) D4 prostaglandins
  7. 7. Diagnostic tests for immediatehypersensitivity■Skin (prick and intradermal) tests.■Measurement of Total IgE andspecific IgE antibodies: measured byELISA.
  8. 8. Treatment A- Avoidance of exposure. B- Symptomatic treatment. C- Immunotherapy
  9. 9. Symptomatic treatment1-Antihistamines which block histamine receptors.2-Chromolyn sodium inhibits mast cell degranulation, by inhibiting Ca++ influx.3-Late onset allergic symptoms, particularly bronchoconstriction which is mediated by leukotrienes, are treated with leukotriene receptor blockers or inhibitors of the cyclooxygenase.4-Symptomatic, although short term, relief from bronchoconstriction is provided by bronchodilators (inhalants).
  10. 10. Type II hypersensitivity ■ Also known as cytotoxic hypersensitivity and may affect a variety of organs and tissues.■ The antigens are normally endogenous, althoughexogenous chemicals (haptens) which can attach to cell membranes can also lead to type II hypersensitivity. ■ Primarily mediated by IgM or IgG classes → ◘Complement mediated lysis. ◘Phagocytes and Killer cells may also play a role (ADCC).
  11. 11. Types A- RBCs lysis:  1- Incompatible blood transfusion.  2- Erythroblastosis faetalis:  3- Autoimmune hemolytic disease. B- WBCs lysis:  1- Granulocytopenia.  2- S.L.E. C- Platelet destruction:
  12. 12. Type III Hypersensitivity (immune (complex hypersensitivity■ It is mediated by soluble immunecomplexes. They are mostly of the IgG,although IgM may also be involved.■ The antigen may be: ■ exogenous (chronic bacterial, viral or parasitic infections). ■ endogenous (non-organ specific autoimmunity: e.g. (SLE).
  13. 13. Mehanism■ The Ag is soluble and not attached to the organ involved.■ Soluble Ag-antibody complexes which pentrate the enothelium of blood vessel and deposited on the vascular basement membrane.■ This will stimulate the complement and chemotactic factors like C5a is released which attract neutrophils which infitrate the area and release lysosomal enzymes leading to destruction of the basement membrane.
  14. 14. Types:Arthus reaction -1:Serum sickness -2:Hypersensitivity pneumonitis -3:Posstreptococcal glomerulonephritis -4Autoimmune disease: RA , SLE -5
  15. 15. Type IV Hypersensitivity■ Type IV hypersensitivity is also known as cellmediated or delayed type hypersensitivity.■ The classical example of this hypersensitivity istuberculin (Montoux) reaction which peaks 48hours after the injection of antigen (PPD or oldtuberculin). The lesion is characterized byinduration and erythema.
  16. 16. ■ Mechanisms of damage in delayed hypersensitivityinclude T lymphocytes and monocytes and/ormacrophages. Cytotoxic T cells cause direct damagewhereas Th1 cells secrete cytokines which activatecytotoxic T cells and recruit and activate monocytes andmacrophages, which cause the bulk of the damage. Thedelayed hypersensitivity lesions mainly contain monocytesand a few T cells.■ Major lymphokines involved in delayed hypersensitivityreaction include monocyte chemotactic factor, Il-2,interferon-gamma, TNF alpha/beta, etc.

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