Kaufmann S H, Brinkmann V
Cell Immunol. 1984 Oct 15;88(2):545-50. doi: 10.1016/0008-8749(84)90186-2.
Cultures of T cells from Listeria monocytogenes-immune mice, macrophages, and heat-killed Listeria organisms produced a factor(s) capable of activating macrophage oxygen metabolism. The activity depended on the presence of Lyt 1+2,3- T cells in the primary culture. Macrophage oxygen metabolism could also be induced by a L. monocytogenes-specific T-cell clone which was recently shown to mediate anti-listerial protection in vivo and to secrete interferon-gamma (IFN-gamma) in vitro. Furthermore, macrophage activation was achieved by recombinant IFN-gamma. It is concluded that acquired resistance to facultative intracellular pathogens--at least in part--depends on the activation of macrophage oxygen metabolism by IFN-gamma derived from specific Lyt 1+2,3- T cells.
来自单核细胞增生李斯特菌免疫小鼠的T细胞、巨噬细胞以及经热灭活的李斯特菌培养物产生了一种能够激活巨噬细胞氧代谢的因子。该活性依赖于原代培养物中Lyt 1+2,3-T细胞的存在。巨噬细胞氧代谢也可由单核细胞增生李斯特菌特异性T细胞克隆诱导,最近研究表明该克隆在体内介导抗李斯特菌保护作用,并在体外分泌γ干扰素(IFN-γ)。此外,重组IFN-γ可实现巨噬细胞的激活。得出的结论是,对兼性细胞内病原体的获得性抗性——至少部分——依赖于源自特定Lyt 1+2,3-T细胞的IFN-γ对巨噬细胞氧代谢的激活。