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Immunity of tuberculosis

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Author(s): Özbal, Y.

Journal: Erciyes Medical Journal
ISSN 1300-199X

Volume: 28;
Issue: 1;
Start page: 25;
Date: 2006;
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Keywords: Immunology | Tuberculosis

ABSTRACT
M.tuberculosis has several structural components that play a role in directing these host-pathogen interactions. The host immune response in M.tuberculosis infection, with emphasis on the roles of macrophages, T lymphocytes and cytokines network in effective protective immunity, as well as acquired immunity with presentation of mycobacterial antigens by MHC I, MHC II and CD1 molecules to T cells are summarized in this review. Humans resist infection with mycobacteria in several ways. First, innate defenses against infection exclude infectious agents or kills them on first contact. Non-adaptive responses are crucial to control infection and hold them in check until acquired immunity can be generated. Adaptive immunity takes several weeks to develop, as T lymphocytes must encounter their specific antigen, proliferate and differentiate into effector cells. Once an adaptive immune response has occurred, the infection usually will have been controlled or pathogen eliminated. When mycobacteria resist the effects of macrophage activation, a characteristic localized inflammatory response called a granuloma develops. Mycobacteria can persist in the cells of the granuloma and persistent bacilli can reactivate to form disease many years to decades after initial infection. Soon after infection, the bacilli are phagocytosed by alveolar macrophages and survive within early phagosomes. Subsequent recruitment of dendritic cells leads to cell-mediated responses involving CD4+ and CD8+TH cells. Macrophage activation is mediated by membrane-bound signals delivered by the inflammatory CD4+TH lymphocytes, as well as by the potent-macrophage activating cytokine INF-g, which is secreted by these cells. Activated macrophages can kill intracellular bacteria, also causing local tissue damage. Inflammatory CD4+ TH lymphocytes produce a range of cytokins and chemokines that not only activate infected macrophages but can also kill senescent macrophages to release engulfed bacteria, recruit fresh macrophages to sites of infection. Delayed-type hypersensitivity reaction is mediated by Inflammatory CD4+TH lymphocytes that either activate local inflammatory responses in the site of antigen depositon or kill tissue cells directly. The delayed-type hypersensitivity is directed by cytokins released by Inflammatory CD4+TH lymphocytes stimulated by antigen. This reaction is identical to protective responses by its mechanism, different only in the source and nature of the antigen.

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