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The host response to infection by tubercle bacilli is primarily cellular: they are phagocytosed by macrophages which are stimulated to produce enzymes and cytokines. On average, the cell-medicated immunity develops within 2-8 weeks after infection. These enzymes kill other tissue cells and the cytokines promote the further infiltration of macrophages. Granuloma form and within a few days of infection, before the onset of acquired immune response, the typical concentric tubercle has formed. This limits local spread of infection and may achieve complete resolution. The specific acquired immune response is largely cell mediated. T-lymphocytes, sensitised by contact with mycobacterial antigen, release lymphokines which activate macrophages to kill tubercle bacilli and inhibit intracellular multiplication. Such sensitised lymphocytes are induced by BCG immunisation. Local tissue damage, characteristic of post-primary tuberculosis, is caused largely by delayed hypersensitivity type reaction to mycobacterial protein antigens. Delayed hypersensitivity is also cell-mediated involving circulating sensitised T-lymphocytes and macrophages. It forms the basis of the tuberculin test. The function of sensitised macrophages and lymphocytes is impaired when patients are immunosuppressed (eg taking immunosuppressive drugs such as corticosteroids, lymphoma, HIV infection) resulting in reduced host defence.
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Pathology
and immunology