Study of respiratory symptoms among sputum positive

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Immune mechanisms
A) Cell-mediated immunity (Acquired cellular resistance) :
Cell- mediated immunity (CMI) can be defined as a beneficial host
response characterized by an expanded population of specific T.
lymphocytes. That, in the presence of microbial antigens, produce
cytokines locally. These cytokines attract monocytes/macrophages from the
blood stream into the lesion and activate them, interferon-v (IFN- y) and
tumor necrosis factor-a (TNF-a) are major macrophage-activating
cytokines (Belosevic et al., 1988 and Celada & Nathan, 1994). INF-yalso
induces interleukin 2 (IL-2) receptors in monocyte macrophages, after
which IL-2 becomes an additional activating cytokine for these phagocytes
(Holter et aI., 1987). Activated macrophages produce reactive oxygen
(Klebanoff, 1988) and nitrogen intermediates (Liew and Cox, 1991),
lysosomal enzymes, and other factors that kill and digest tubercle bacilli
(Remick and Friedland, 1997). Acquired cellular resistance (ACR) is
characterized by the presence of a local population of activated
(microbicidal) macrophages, produced by eMI (Dannenberg, 1989) (i.e
By the cytokines ofantigen-stimulated lymphocytes) (Barnes et al., 1990).
In the 1960, Machaness showed that acquired cellular resistance
once produced, was non specific. Activated macrophages could destroy or
inhibit many types of facultative intracellular bacteria, not just the type that
caused their activation. However, once these activated macrophages have
disappeared, following the healing of the primary infection, only the
specific bacterial species could rapidly produce them a gain. This rapid
"recall" response is due to the presence ofexpanded populations oflong
lived (i.e. non dividing) recirculating Th. lymphocytes (memory cells) with
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