Kimura Y, Yamada K, Sakai T, Mishima K, Nishimura H, Matsumoto Y, Singh M, Yoshikai Y
Laboratory of Host Defense and Germfree Life, Research Institute for Disease Mechanism and Control, Nagoya University School of Medicine, Japan.
Int Immunol. 1998 Feb;10(2):117-30. doi: 10.1093/intimm/10.2.117.
Protection against infection with Listeria monocytogenes depends primarily on Listeria-specific T cells. We show here that CD4+ TCR alphabeta+ T cells are capable of recognizing the mycobacterial heat shock protein (HSP) 70, that appears in the peritoneal cavity of F344 rats infected i.p. with L. monocytogenes. The HSP70-reactive CD4+ T cells recognized a peptide comprising 234-252 residues as present in the 70 kDa HSP of Mycobacterium tuberculosis in the context of RT1.B MHC class II molecules. Analysis of TCR Vbeta gene expression with RT-PCR revealed that the HSP70-reactive CD4+ T cells predominantly used the Vbeta16 gene segment, whereas the heat-killed Listeria (HKL)-specific T cells expressed a diverse set of Vbeta gene segments. In contrast to the HKL-specific T cells producing IFN-gamma, the HSP70-reactive CD4+ T cells produced TGF-beta1 and IL-10 but neither Th1- or Th2-type cytokines. Adoptive transfer with HSP70-reactive T cells rendered rats susceptible to listerial infection. Collectively, these results proposed that the HSP70-reactive CD4+ T cells appearing during rat listeriosis may be involved in termination of Th1 cell-mediated excessive inflammation after the battle against L. monocytogenes has been won.
对单核细胞增生李斯特菌感染的抵抗力主要取决于李斯特菌特异性T细胞。我们在此表明，CD4+ TCR αβ+ T细胞能够识别在经腹腔感染单核细胞增生李斯特菌的F344大鼠腹腔中出现的分枝杆菌热休克蛋白（HSP）70。HSP70反应性CD4+ T细胞在RT1.B MHC II类分子的背景下识别包含结核分枝杆菌70 kDa HSP中234 - 252位残基的肽段。用RT-PCR分析TCR Vβ基因表达表明，HSP70反应性CD4+ T细胞主要使用Vβ16基因片段，而热灭活李斯特菌（HKL）特异性T细胞表达多种Vβ基因片段。与产生IFN-γ的HKL特异性T细胞不同，HSP70反应性CD4+ T细胞产生TGF-β1和IL-10，但不产生Th1型或Th2型细胞因子。用HSP70反应性T细胞进行过继转移使大鼠易受李斯特菌感染。总体而言，这些结果表明，在大鼠李斯特菌病期间出现的HSP70反应性CD4+ T细胞可能在战胜单核细胞增生李斯特菌后参与终止Th1细胞介导的过度炎症反应。
