[Frontiers in Bioscience 3, c27-33, May 1, 1998] |
LURIEíS TUBERCLE-COUNT METHOD TO TEST TB VACCINE EFFICACY IN RABBITS
Departments of Environmental Health Sciences, Molecular Microbiology and Immunology, and Epidemiology, School of Hygiene and Public Health; and the Department of Pathology, School of Medicine, The Johns Hopkins University, Baltimore, Maryland 21205
Received 3/9/98 Accepted 3/14/98
5. IMMUNE MECHANISMS CONTROLLING THE PROGRESS OF THE EARLY MICROSCOPIC PULMONARY LESION (13,14,17,18)
A small microscopic tubercle is produced wherever the bacillus multiplies appreciably in an alveolar macrophage (AM). The alveolar macrophage eventually dies, and blood-borne monocyte/macrophages emigrate from the bloodstream into the site and ingest the bacilli released from the AM. These new macrophages are not activated, so the bacillus multiplies intracellularly in a logarithmic fashion. In rabbits that have inhaled human-type bacilli, most of these early lesions never reach grossly visible size, because acquired immunity soon develops to antigens secreted by the bacillus: a) The hostís tissue-damaging delayed-type hypersensitivity (DTH) reaction kills the nonactivated macrophages in which the bacillus is multiplying, thereby forming the lesionís solid caseous center(s) in which the bacillus cannot multiply; and b) cell-mediated immunity (CMI) activates the macrophages surrounding the caseous center(s) and some of these activated macrophages ingest the bacilli that escape from the caseous center(s). Since such activated macrophages can inhibit and destroy tubercle bacilli, the early microscopic lesion is often arrested at this point of its development. The acquired immunity just described converts the tuberculin reaction, but the host will not show any other evidence of clinical disease unless the early lesion continues to progress.