Delayed type hypersensitivity (DTH) reactions are antigen-specific, cell-mediated immune responses which, depending on the antigen involved, mediate beneficial (resistance to viruses, bacteria, fungi, and tumors) or harmful (allergic dermatitis, autoimmunity) aspects of immune function. Cutaneous DTH reactions are initiated when CD4 memory T cells are activated by Langerhans cells and other antigen-presenting cells in the skin. Upon activation, CD4 T cells release inflammatory mediators which recruit effector cells to the site of antigen administration. While the monocyte/macrophage is thought to be the major effector cell in this model, CD8+ cytolytic T cells, and NK cells are also thought to serve as effector cells in DTH reactions. Activated effector cells mount an inflammatory response which results in the elimination of antigen and the extravasation of plasma accompanied by selling at the site of challenge. The magnitude of the response to the antigen is measured as an increase in swelling at the site of challenge.
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