Miyoshi-Akiyama T, Fujimaki W, Yan X J, Yagi J, Imanishi K, Kato H, Tomonari K, Uchiyama T
Department of Microbiology and Immunology, Tokyo Women's Medical College, Shinjuku-ku, Japan.
Microbiol Immunol. 1997;41(4):345-52. doi: 10.1111/j.1348-0421.1997.tb01211.x.
We previously reported that Yersinia pseudotuberculosis-derived mitogen (YPM) acts as a superantigen to human T cells. In this study, we assessed the superantigenicity and toxicity of YPM using murine experimental models. YPM activated T cells to produce interleukin-2 in a major histocompatibility complex class II molecule-dependent manner. The T-cell blasts induced by YPM expressed T-cell receptor (TCR) beta-chain variable region (Vbeta)7, Vbeta8.1, Vbeta8.2 and Vbeta8.3. The injection of YPM into mice pre-sensitized with D-galactosamine induced lethal shock. This shock was blocked by the injection of monoclonal antibodies (mAbs) to CD4, TCR Vbeta7 plus Vbeta8, tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma), but not by injection to CD8 or unrelated Vbeta. These results indicate that YPM-induced shock requires the presence of CD4+ T cells bearing TCR Vbeta7 and Vbeta8, and that endogenous TNF-alpha and IFN-gamma mediate the lethal effects.
我们之前报道过，假结核耶尔森菌衍生的促有丝分裂原（YPM）可作为人类T细胞的超抗原。在本研究中，我们使用小鼠实验模型评估了YPM的超抗原性和毒性。YPM以主要组织相容性复合体II类分子依赖性方式激活T细胞产生白细胞介素-2。YPM诱导的T细胞母细胞表达T细胞受体（TCR）β链可变区（Vβ）7、Vβ8.1、Vβ8.2和Vβ8.3。向用D-半乳糖胺预先致敏的小鼠注射YPM会诱导致死性休克。这种休克可通过注射针对CD4、TCR Vβ7加Vβ8、肿瘤坏死因子-α（TNF-α）和干扰素-γ（IFN-γ）的单克隆抗体（mAb）来阻断，但注射针对CD8或不相关Vβ的抗体则不能阻断。这些结果表明，YPM诱导的休克需要存在携带TCR Vβ7和Vβ8的CD4 + T细胞，并且内源性TNF-α和IFN-γ介导了致死效应。
