Immune mechanisms in the pathogenesis of pulmonary tuberculosis.
The pathogenesis of pulmonary tuberculosis and the beneficial and detrimental effects of the host's cell-mediated immune response in this disease are reviewed. Tubercle bacilli are hardly facultative intracellular pathogens that live and multiply in nonactivated macrophages. Before tubercle bacilli can be destroyed by macrophages, these cells must be activated by T lymphocytes and their lymphokines. Such activation is the essence of cell-mediated immunity. Cell-mediated immunity also has a detrimental component, called delayed-type hypersensitivity. This component causes caseous necrosis of host tissues whenever the bacillary antigens reach high levels. Such levels occur intracellularly in macrophages of highly susceptible hosts and extracellularly in liquefied caseous foci of resistant hosts. Vaccines containing antigens that create more cell-mediated immunity and less delayed-type hypersensitivity are greatly needed.
Dannenberg
A M
AM
Department of Environmental Health Sciences, School of Hygiene and Public Health, Baltimore, Maryland 21205.
D001428:Bacterial Vaccines; D006801:Humans; D006968:Hypersensitivity, Delayed; D007111:Immunity, Cellular; D008213:Lymphocyte Activation; D008222:Lymphokines / Q000276:immunology; D008262:Macrophage Activation; D008264:Macrophages / Q000276:immunology / Q000382:microbiology; D009169:Mycobacterium tuberculosis / Q000276:immunology; D014374:Tuberculin Test; D014397:Tuberculosis, Pulmonary / Q000209:etiology* / Q000276:immunology / Q000473:pathology
D001428:Bacterial Vaccines; D008222:Lymphokines