Immunopathogenesis of delayed-type hypersensitivity.

Cell-mediated immunity is defined as a beneficial host response characterized by an expanded population of specific T cells, which, in the presence of antigens, produce cytokines locally. The activation and recruitment of cells into an area of inflammation is a crucial step in the development of DTH responses. DTH is immunologically a process similar to cell-mediated immunity, involving T cells and cytokines. CD4 T helper (Th) 1 cells, differentiated from naive Th cells by IL-12 and IL-18 produced from macrophages, play a regulatory role in the expression of DTH and activation of macrophages via interferon gamma generated by Th1 and natural killer cells. Macrophages accumulate at the site of DTH and become activated through the CD4 Th1 cell-cytokine-macrophage axis. However, DTH leads to pathologic responses, such as granulomatous inflammation, calcification, caseation necrosis, and cavity formation. Granulomas usually form as a result of the persistence of a nondegradable product or as the result of DTH responses. DTH is also required for host defense against etiologic agents, such as Mycobacterium tuberculosis. The expression of cell-mediated immunity/DTH is a double-edged sword that may contribute to both clearance of the etiologic agent and tissue damage.