T lymphocyte-macrophage interactions in cellular antibacterial immunity.

Acquired resistance to facultative intracellular bacteria depends on a bicellular mechanism whereby specific T lymphocytes activate macrophages for enhanced bacteriocidal capacity. In vivo, protection is paralleled by delayed-type hypersensitivity. In vitro correlates are specific T lymphocyte proliferation and interleukin induction. Macrophage activation results from complex cell interactions involving both T lymphocytes and macrophages. Although such interactions are not yet fully understood, it appears likely that interleukin-facilitated collaboration between Lyt 1 and Lyt 123 T lymphocytes is required. Most probably, H2-restricted interactions between antigen-presenting mononuclear phagocytes and Lyt 1 T lymphocytes induce secretion of interleukins which further recruit additional Lyt 1 T lymphocytes from the Lyt 123 T lymphocyte set. In this way, the pool of Lyt 1 T lymphocytes capable of attracting and activating macrophages at the site of bacterial and implantation via lymphokines (macrophage activating factor, migration inhibition factor) could be markedly enhanced.