Kaufmann S H
Infect Immun. 1983 Mar;39(3):1265-70. doi: 10.1128/iai.39.3.1265-1270.1983.
The capacity of the murine Listeria monocytogenes-specific T cell clone 9-36-1 and of lymphokines derived therefrom to induce antibacterial protection in vivo was studied. Clone 9-36-1 was stimulated to proliferate and to produce lymphokines by in vitro culture with syngeneic accessory cells and heat-killed L. monocytogenes. Although 9-36-1 cells were highly active in vitro, intravenous transfer of the cells resulted in marginal protection against a systemic infection with L. monocytogenes. In contrast, 9-36-1 cells injected subcutaneously together with L. monocytogenes into the footpad induced marked protection in syngeneic, but not in allogeneic, mice. Multiplication of Salmonella typhimurium was not reduced by the T cell clone. Studies with 51Cr-labeled T cells indicated that the low activity of intravenously transferred cells was due to an altered migration pattern. Lymphokines produced by 9-36-1 cells in vitro induced protection against L. monocytogenes in syngeneic recipient mice. Lymphokine-induced protection was also demonstrable in allogeneic recipients and against S. typhimurium. These findings suggest that the L. monocytogenes-specific T cell clone 9-36-1, although unable to immigrate into sites of bacterial deposition, had retained its ability to mobilize antibacterial defense mechanisms once present at the site of reaction.
研究了小鼠单核细胞增生李斯特菌特异性T细胞克隆9-36-1及其衍生的淋巴因子在体内诱导抗菌保护的能力。通过与同基因辅助细胞和热灭活的单核细胞增生李斯特菌进行体外培养，刺激克隆9-36-1增殖并产生淋巴因子。尽管9-36-1细胞在体外具有高活性，但静脉注射这些细胞对单核细胞增生李斯特菌的全身感染仅提供了微弱的保护。相反，将9-36-1细胞与单核细胞增生李斯特菌一起皮下注射到足垫中，可在同基因小鼠而非异基因小鼠中诱导显著的保护作用。鼠伤寒沙门氏菌的增殖未被T细胞克隆所抑制。对51Cr标记的T细胞的研究表明，静脉注射细胞的低活性是由于迁移模式改变所致。9-36-1细胞在体外产生的淋巴因子可在同基因受体小鼠中诱导对单核细胞增生李斯特菌的保护作用。在异基因受体中以及对鼠伤寒沙门氏菌也可证明淋巴因子诱导的保护作用。这些发现表明，单核细胞增生李斯特菌特异性T细胞克隆9-36-1虽然无法迁移到细菌沉积部位，但一旦存在于反应部位，仍保留其调动抗菌防御机制的能力。
