Roles of cytotoxic delayed-type hypersensitivity and macrophage-activating cell-mediated immunity in the pathogenesis of tuberculosis.

摘要: The tubercle bacillus is a facultative intracellular parasite that grows well in non-activated macrophages. When large numbers of these bacilli have grown intracellularly within such macrophages, cytotoxic immune response, herein called tissue-damaging (or necrotizing) delayed-type hypersensitivity (DTH), kills the macrophages (and usually some surrounding tissue), forming caseous center developing tubercle. In solid caseum, may survive, but do not multiply. escape from edge they are rapidly ingested by nearby viable If been activated, again multiply intracellularly, and response bacilli-laden thus enlarging center. hosts develop poor activation this process repeated until much lung destroyed. can good (by cytokines antigen-specific T cells), cell-mediated immunity (CMI), centers become surrounded activated which ingest destroy escaping caseum. This arrest disease. Unfortunately, liquefy resistant hosts. liquefied menstruum, grow extracellularly (for first time during course disease), reaching tremendous numbers. to numerous their tuberculin-like products causes tissue necrosis, including erosion walls small bronchi, results cavity formation. From cavities, spread other parts environment. extracellular multiplication caseum main reason why tuberculosis perpetuates itself mankind. It also antimicrobial drug-resistant bacillary strains develop. To elucidate various mechanisms involved macrophage activation, caseation, liquefaction major challenge for researchers today.