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Delayed-type hypersensitivity (DTH) is a form of immune response classified as Type IV hypersensitivity. It is cell-mediated rather than antibody-mediated and typically manifests 24–72 hours after exposure to an antigen. DTH plays a critical role in host defense against intracellular pathogens and is also involved in immunopathology associated with autoimmune diseases, contact dermatitis, drug reactions, and transplant rejection. The reaction serves both protective functions (eliminating infected or altered cells) and pathological roles when excessive or misdirected. The mechanism involves sensitization and elicitation phases, with key cellular components including CD4+ Th1 cells, macrophages, dendritic cells, keratinocytes, and endothelial cells. Major mediators include IFN-gamma, TNF-alpha, and IL-2. Common clinical manifestations include the tuberculin skin test reaction, contact dermatitis, and drug-induced exanthems. While essential for pathogen clearance—especially intracellular microbes—excessive or misdirected DTH can cause significant tissue damage.
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