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Hypersensitivity reactions

Hypersensitivity reactions. Hypersensitivity reactions are grouped into four types according to the effector mechanisms producing the reaction: Immediate, IgE /mast cell-mediated Antibody-mediated Immune complex-mediated T cell-mediated.

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Hypersensitivity reactions

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  1. Hypersensitivity reactions Hypersensitivity reactions are grouped into four types according to the effector mechanisms producing the reaction: Immediate, IgE/mast cell-mediated Antibody-mediated Immune complex-mediated T cell-mediated An adaptive immune response to innocuous molecules that causes inflammation and tissue damage

  2. Immediate hypersensitivity(Type I) • Production of IgE antibodies in response to an antigen  binding of IgE to Fc receptors of mast cells  cross-linking of bound IgE by the antigen  release of mast cell mediators • Mast cell mediators- vasoactive amines, lipid mediators and cytokines result in: • Rapid increase of vascular permeability (histamine, PGs) • Smooth muscle contraction that occurs within minutes (histamine, LTs) • Recruitment of neutrophils and eosinophils- late phase reaction (cytokines TNF and IL-4). Th2 cells recruit eosinophils (IL-5) and increase mucus secretions (IL-13) • Local tissue damage by neutrophils and eosinophils (proteases) • IgE production is a result of a dominant Th2 response against the allergen for an unknown reason (genetic basis).

  3. Immediate hypersensitivity(Type I) Immediate hypersensitivity reactions are called allergy or atopy. An individual developing this reaction is said to be atopic. Antigens causing a state of immediate hypersensitivity/allergy are called allergens. In developed countries 10-40% of the population are allergic to one or more environmental allergens! • Mast cells are always coated by IgE through FcεRI high affinity to ε chain of IgE. • Mast cell coating with IgE is called “sensitization” – Mast cells become sensitive to activation by the encounter with that antigen. The evolutionary purpose of mast cells is in the defense against helminthes, unfortunately, they are also responsible for these allergic reactions

  4. Often IgG or IgM autoantibodies are involved (failure of self tolerance) • Some cases involve antibodies produced against a foreign antigen. For example: poststreptococcal glomerulonephritis and Rheumatic fever. Antibodies directed against cell or tissue antigens, damage or impair their function • IgG1 and IgG3 subclasses bind Fc receptors on macrophages and neutrophils leukocyte activation  inflammation. • IgM, IgG1 and IgG3 activate the classical pathway of complement  leukocyte recruitment  inflammation. • ROS, lysosomal enzymes bring about the tissue damage. Antibody-mediated hypersensitivity(Type II)

  5. Deposition in sites of turbulence and high pressure; • - Vessel branches (vasculitis) • - Kidney glomeruli (nephritis) • - Synovium(arthritis) Antibodies form complexes with the antigens and deposit in blood vessels causing inflammation and injury • Therapy intends to limit inflammation-corticosteroids • and reduce circulating antibodies and immune complexes - • plasmapheresis. Immune complex mediated-hypersensitivity (Type III)

  6. Contact sensitivity to chemicals • T cell response against Mycobacterium tuberculosis chronic (not able to be eradicated)  granulomatous inflammation  tissue injury • CTL response to HBV infected hepatocytes  liver injury • Superantigens polyclonal T cell stimulation  systemic shock Delayed type hypersensitivity reactions are mediated by CD4+or CD8+ CTLs A result of autoimmunity or a response to environmental antigens Usually restricted to a tissue, not systemic. However, chronic and progressive T cell-mediated hypersensitivity(Type IV) • The mechanism of injury to the tissue is the same as what T cells use to eliminate cell-associated pathogens. CTL- direct killing. Th1- Macrophage activation through IFN-γ. • Therapy is designed to reduce inflammation- corticosteroids, cytokine antagonists (MAB targeting TNF in RA and IBD, IL-2), immunosuppressive agents acting on T cells.

  7. T-cell mediated hypersensitivity reaction (type IV) Contact sensitivity to poison ivy

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