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Regulation of immune response in hole body and intestinal mucosa by oral administration of staphylococcal enterotoxin B (SEB)

口服葡萄球菌肠毒素B（SEB）对孔体和肠粘膜免疫反应的调节

基本信息

批准号：
09670542
负责人：
TSUJIKAWA Tomoyuki
金额：
$ 2.18万
依托单位：
Shiga University of Medical Science
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1997
资助国家：
日本
起止时间：
1997 至 1999
项目状态：
已结题

项目摘要

We have been elucidated that oral SEB administration prevented the onset of DSS induced colitis, and influence of clonal deletion designated by Vβ8T -cells. We evaluated the effect of oral SEB administration on TCR α KO mice. (Experiment 1) Simultaneous administration of SEB ameliorated DSS induced colitis on TCR α KO mice, following prolonged survival time. Although serum Ig M of mice administered DSS increased more than that of control, the cell fractions of CD4ィイD1+ィエD1TCRVβィイD1dimィエD1T-cells and CD4ィイD1+ィエD1TCRVβィイD1dimィエD1T-cells did not change with or without SEB oral administration. (Experiment 2) Although TCR α KO mice have been given SEB for 9 weeks, the incidence of colitis did not decrease and the cell fractions of CD4ィイD1+ィエD1TCRVβィイD1dimィエD1T-cells also did not change. It was suggested that CD4ィイD1+ィエD1TCRVβィイD1dimィエD1T-cell may influence the onset of the colitis on TCR α KO mice. We elucidated that preventive effect of SEB on DSS induced colitis of TCR α KO mice. Therefore, it is suggested that TCRαィイD1-ィエD1βィイD1+ィエD1 cells which express the Vβ region corresponding SEB may play an important role on the onset of DSS induced colitis on TCR α KO mice. However, it was difficult to induce oral tolerance by SEB under condition of continuing local inflammation such as colitis of TCR α KO mice.

我们已经阐明口服SEB预防DSS诱导的结肠炎的发作，以及由Vβ 8 T-细胞指定的克隆缺失的影响。我们评估了口服SEB对TCR α KO小鼠的影响。（实验1）同时给予SEB可改善TCR α KO小鼠中DSS诱导的结肠炎，延长存活时间。尽管DSS给药小鼠的血清IG M比对照组增加更多，但在SEB口服给药或未口服给药的情况下，CD 4 + D1+ TCRV β CD 4 + D1细胞的细胞分数没有变化。（实验2）虽然TCR α KO小鼠已给予SEB 9周，但结肠炎的发生率并未降低，CD 4 + CD 4 + D1+ CD 4 + D1+ TCRV β CD 4 + D1+ CD 4 + D1 + TCRV β CD 4 + D1 + D1 + T细胞的细胞分数也未发生变化。提示CD 4 ~+~ D1 TCRV β ~+~ D1 ~ D1 T细胞可能影响TCR α KO小鼠结肠炎的发病。本研究阐明了SEB对DSS诱导的TCR α KO小鼠结肠炎的预防作用。因此，表明表达Vβ区相应SEB的TCRα κ D1-κ D1β κ D1+ κ D1细胞可能在DSS诱导的TCR α KO小鼠结肠炎的发病中起重要作用。但在TCR α KO小鼠结肠炎等持续局部炎症的情况下，SEB难以诱导口服耐受。