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6 . Immunology

6 . Immunology. By. Dr. Emad AbdElhameed Morad. Lecturer of Medical Microbiology and Immunology. HYPERSENSITIVITY REACTIONS (ALLERGY). Definition. Exaggerated immune response to an antigen leading to tissue damage. Type I, II, III are antibody mediated hypersensitivity reactions.

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6 . Immunology

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  1. 6. Immunology By Dr. Emad AbdElhameed Morad Lecturer of Medical Microbiology and Immunology

  2. HYPERSENSITIVITY REACTIONS (ALLERGY)

  3. Definition • Exaggerated immune response to an antigen leading to tissue damage. • Type I, II, IIIare antibody mediated hypersensitivity reactions. • Type IVis cell mediated hypersensitivity reaction. Types

  4. Type I hypersensitivity • It is also called immediate hypersensitivity. • Pathogenesis: • On first exposure to the antigen (allergen), the allergen is taken by the macrophages, processed and presented on its surface to stimulate TH0 which will differentiate to TH2 cells. • TH2 cells will secrete IL4 that will activate B lymphocytes to secrete antibody of IgE class. • IgE attaches to the mast cells by its Fc portion because it is cytotropic.

  5. On second exposure to the same allergen, it binds with IgE present on the surface of mast cells leading to mast cell degranulation. • Mast cell degranulation results in release of chemical mediators like histamine. • These mediators will cause the following effects: • Smooth muscle contraction especially in bronchi leading to bronchospasm. • Increased mucous secretion. • Vasodilatation of capillaries leading to: • Hypotension • Urticaria

  6. Type I hypersensitivity

  7. Clinical types: • Systemic form (anaphylaxis): • Common allergen is drug like penicillin or insect venom. • Manifestations include: • Bronchospasm • Shock due to hypotension • Urticaria Urticaria

  8. Note that the tendency to develop atopy is inherited among families • Local form (atopy): • Allergens may be: • Inhalants:pollens, fungal spores • Ingestants:milk, fish, egg • Contactants:wool, animals fur • Injectants:drugs • Manifestations are variable: • Bronchi:bronchospasm • Nose:rhinitis • GIT:diarrhea • Skin:urticaria • Eye:conjunctivitis

  9. Diagnosis: • History taking. • IgE level is increased in blood. • Skin test: • Intradermal injection of the allergen in a hypersensitive patient results in erythema and wheal at the site of injection within 15-20 minutes.

  10. Treatment: • Avoid exposure to the allergen. • Drugs: • Antihistaminic drugs • Corticosteroids • Epinephrine • Sodium chromoglycate • Hyposensitization: • Long-weekly administration of the allergen by subcutaneous injection of gradually increasing doses of the allergen.

  11. Type II hypersensitivity • It is also called cytolytic hypersensitivity. • Pathogenesis: • Occurs when antibodies (IgG or IgM) react with antigens on cell surface leading to cell lysis by several mechanisms: • Complement activation. • Opsonization by macrophages. • Antibody dependent cellular cytotoxicity (ADCC) by natural killer cells. • Clinical example: • Mismatched blood transfusion.

  12. Type II hypersensitivity

  13. Type III hypersensitivity • It is also called immune complex mediated hypersensitivity. • Pathogenesis: • This type of hypersensitivity occurs when small soluble antigen antibody complexes are formed in the blood. • These immune complexes will activate the complement with consequent production of C3a and C5a. • C3a and C5a will cause mast cell degranulation with release of histamine.

  14. Histamine causes Vasodilatation of capillaries leading to deposition of the immune complexes on the vascular basement membrane. • C5a is also chemotactic.It attracts phagocytic cells. The attracted neutrophils will release lysosomal enzymes which destroy the basement membrane. • Platelet aggregation with formation of microthrombi leading to local ischemia and tissue necrosis. • Clinical example: • Post streptococcal glomerulonephritis

  15. Type III hypersensitivity

  16. Type IV hypersensitivity • It is also called delayed hypersensitivity. • Pathogenesis: • On first exposure to the antigen, the antigen is taken by the macrophages, processed and presented on its surface to stimulate TH0 cells that will differentiate into TH1 cells. • On second exposure to the same antigen, TH1 cells will secrete large amounts of: • IL-2 that activates CD8 cytotoxic T lymphocytes. • Interferon γ which activates macrophages.

  17. Both cells will infiltrate the site of the antigen and cause tissue damage. • Manifestations occur hours or days after exposure to the antigen (Delayed). • Clinical example: • Contact dermatitis that occurs due to contact of the skin with chemical substances like hair dyes, cosmetics, soap, neomycin skin ointment and poison ivy. Poison ivy

  18. Type IV hypersensitivity

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