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Type I hypersensitivity occurs when IgE antibodies bind to allergens on mast cells and basophils, triggering degranulation and release of histamine and inflammatory mediators. This immediate reaction manifests within minutes of re-exposure in previously sensitized individuals, causing symptoms ranging from mild itching to severe anaphylaxis in conditions like asthma and food allergies.

Type II hypersensitivity involves IgG or IgM antibodies binding to antigens on cell surfaces, initiating phagocytosis and cell lysis through complement activation or antibody-dependent cell-mediated cytotoxicity. Examples include mismatched blood transfusions and autoimmune hemolytic anemia, where the immune system mistakenly destroys the body's own cells.

Type III hypersensitivity occurs when antigen-antibody complexes deposit in tissues, triggering inflammation and tissue damage. Conditions like rheumatoid arthritis and glomerulonephritis result from these immune complexes accumulating in joints and kidneys, causing chronic inflammation and progressive organ dysfunction throughout affected areas.

Type IV hypersensitivity is delayed because symptoms appear 12-72 hours after allergen exposure, unlike immediate reactions. This cell-mediated response involves T cells reacting to antigens and releasing gamma-interferon, causing inflammation. Contact dermatitis and transplant rejection are common examples of this delayed immune response.

Immediate hypersensitivity (Type I) occurs within minutes through IgE antibodies and mast cell degranulation, while delayed hypersensitivity (Type IV) develops over 12-72 hours through T cell-mediated responses. Immediate reactions cause rapid symptoms like hives and anaphylaxis, whereas delayed reactions produce localized inflammation such as contact dermatitis.

Initial exposure to specific allergens stimulates substantial production of IgE antibodies, which adhere to mast cells and basophils. Upon re-exposure, the allergen binds to these pre-existing IgE antibodies, causing the cells to degranulate and release histamine and other inflammatory mediators that produce allergic symptoms.

Types I, II, and III hypersensitivities are antibody-mediated, involving IgE, IgG, or IgM antibodies binding to antigens or forming immune complexes. Type IV hypersensitivity is cell-mediated, relying on T cells reacting to antigens and releasing gamma-interferon without antibody involvement, making it the only non-antibody-mediated hypersensitivity type.