[The immunology of mycobacterial diseases]

Protection and pathogenesis of tuberculosis greatly depend on specific T lymphocytes. Recent evidence suggests the existence of at least two pathways of acquired specific resistance to M. tuberculosis infection: The first consists of cytokine-mediated activation of infected host cells by protective CD4+ T cells, which are currently believed to mediate antimicrobial activity via the release of macrophages activating cytokines such as IFN-gamma and TNF-alpha. The second involves the lysis of these infected cells by cytotoxic effector CD4+ T cells, which is class II MHC restricted, requires cell-to-cell contact mediated by the ICAM-1 and LFA-1 ligand pair, and appears to be independent of lymphotoxins and through the direct cell interaction by adhesion molecules such as LFA-1 and ICAM-1 but not cytokines. On the other hands, gamma delta T cells might be part of the primary response to infection with live M. tuberculosis. gamma delta T cells have the potential to express cytotoxicity for mononuclear phagocytes pulsed with mycobacterial antigens, and are capable of secreting a variety of cytokines, including IL-2 and IFN-gamma. Intracellular killing mechanisms by activated macrophages are still unknown. Recently, increasing attention has been focused on the role of NO as a mediator of a number of physiological reaction. Activated macrophages appear to exhibit some antimicrobial actions as well as antitumor effects via generation of NO, which depends on the L-arginine oxidation pathway. However, it is still unknown whether or not human macrophages generate NO radicals.(ABSTRACT TRUNCATED AT 250 WORDS)