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Hypersensitivity Reactions:

Hypersensitivity Reactions:. Hypersensitivity reactions : I nflammatory immune responses induced by repeated antigen exposure resulting in host tissue damage. Allergen : is a nonparasitic antigen capable of stimulating hypersensitivity reactions.

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Hypersensitivity Reactions:

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  1. Hypersensitivity Reactions:

  2. Hypersensitivity reactions: Inflammatory immune responses induced by repeated antigen exposure resulting in host tissue damage. • Allergen: • is a nonparasitic antigen capable of stimulating hypersensitivity reactions. • An antigen that produces a vigorous immune response in which the immune system fights a threat that is harmless to the body.

  3. Types of Hypersensitivity: • Four groups: according to mechanism of action into • Type I (Immediate hypersensitivity). • Type II (Cytotoxic hypersensitivity). • Type III (Immune complex hypersensitivity). • Type IV (Cell-mediated hypersensitivity) (delayed hypersensitivity).

  4. Examples of Allergen: • Exogenous: • Animal products: fur and dander, cockroach calyx, wool, dust mite excretion • Drugs ( penicillin, sulfonamides) • Food : Egg albumen, Corn, legumes (peanuts, soybeans), milk, and seafood. • Insect venom. • Mold spores. • Plant pollens( hay fever) • Endogenous: Self antigen.

  5. Type I Hypersensitivity: • Known as allergic or immediate hypersensitivity. • The reaction takes 15-30 minutes to appear. • It could appear as a delayed response (10-12 hours later). • Examples: Eczema, Urticaria , Hay fever, Asthma.

  6. Tow types according to the site of reaction: • Localized reaction: Skin, eye, Nasopharynx, Broncho pulmonary or GIT. • Systemic reaction: In Bloodstream: venom or toxin. Lethal effect.

  7. Mast cells • Originate from the bone marrow and are scattered in the connective tissues of the body, especially skin, near blood vessels, respiratory system, and digestive tract). • very similar to basophils (have granules that contains allergy mediators)

  8. Mechanism of Type I Hypersensitivity: • Sensitization phase: • Exposure to allergen. • Isotype switching to IgE • Sensitization of Mast cell by IgE (FcεRI). • Effector phase: • IgE Cross-linking. • Mast cell degranulation and release of vasoactive amines, lipids and cytokines and attraction of eosinophils.

  9. Mast cell inflammatory mediators: • Biogenic amines ( histamines): • Bronchiole constriction, and mucus secretion from Goblet cell. • Vasoconstriction and capillary endothelial vasodilation ; increased vascular permeability (fluid loss and shock).

  10. Lipid mediators: • Leukotriene; similar to histamine effect. • PAF(platelet aggregation): micro thrombosis • Prostaglandins D2:edema and pain. • Cytokines: TNF.

  11. Localized reaction in Skin: UrticariaEczema

  12. Type II Hypersensitivity: • Known as Cytotoxic Hypersensitivity. • Allergen could be: • Endogenous: Cell surface proteins • Exogenous: Drugs adsorbed onto cell membrane.

  13. IgG , IgM, Complement, and Cytotoxic cells are involved in this type of inflammation. • Sites of occurrence of Type II reactions: • On cell surface (Example: RBCs). • Within extracellular matrix (Example: Basement membrane).

  14. Examples on Type II Hypersensitivity: • Alloimmune hemolytic anemia: • Erythroblastosis fetalis (maternal IgG X fetal RBCs) • Alloimmune hemolytic anemia: Blood transfusion anemia(recipient IgMagainst donor RBCs) • Goodpasture’s syndrome (kidneys & lungs). • Graves Disease ( Antibodies against TSH receptors) leading to activation.

  15. Recipient

  16. Type III Hypersensitivity: • Soluble immune Complex hypersensitivity. (IgG- short peptide or IgG- animal sera). • Lead to inflammation at the site of their deposition. • Types of Allergen: • Exogenous: e.g. animal sera. • Endogenous: soluble self antigens.

  17. Mechanism of type III hypersensitivity reaction: • Ag-Ab (IgG) complexes accumulate and deposit (usually in the endothelium) leading to complement activation and neutrophil attraction (C3a, C4a, C5a).

  18. Two types: • Localized (Arthus reaction) example: in skin: Intradermal injection of antigen in skin; necrotizing vasculitis. • Systemic(Serum sickness): Wide dissemination of immune complexes.

  19. Clinical Examples: • Serum sickness disease associated with: -Some types of food allergy. -Prophylactic vaccine (animal antisera). Symptoms develop after 7-10 days and is self-limiting after clearance of the antigen. • Systemic lupus erythematosus (self antigens). • Rheumatoid arthritis (self antigens).

  20. TypeIV Hypersensitivity: • known as cell mediated (CD4 or CD8)or delayed type hypersensitivity. • Antibodies are not involved. • The classical example of this hypersensitivity is tuberculin (Mantoux) reaction which peaks 48hours after the injection of antigen (tuberculin).

  21. Three types: • Contact dermatitis: toxic sensitizer absorbed through epidermis, bind self proteins & form neoantigen . • Delayed type hypersensitivity(DTH): Granulomatous inflammation, not limited to the dermis. Usually due to pathogens e.g. M. tuberculosis. • T cell mediated cytotoxicity: caused by CD8T lymphocytes.

  22. Contact dermatitis

  23. Clinical example: • Tuberculin (Mantoux) test(DTH)

  24. Erythema induratum (Bazin disease): nodules in the legs due to sensitivity to some pathogens e.g. M.tuberculosis

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