Wegmann D R, Gill R G, Norbury-Glaser M, Schloot N, Daniel D
Barbara Davis Center for Childhood Diabetes, University of Colorado Health Sciences Center, Denver 80262.
J Autoimmun. 1994 Dec;7(6):833-43. doi: 10.1006/jaut.1994.1066.
Insulin-specific T cells have been found to be present in high frequency among nominally islet-cell-specific T cells in the islet infiltrates that accumulate in NOD mice. In a previous report in which clones obtained from 7- and 12-week-old mice were examined, we identified a 15-residue peptide of the B chain as the dominent epitope for this response. Despite the fact that the response to insulin appears to be directed toward this single peptide, diverse TCR V beta usage was observed. That insulin-specific T cells contribute to beta cell damage is suggested by the fact that all clones tested could mediate beta cell destruction upon adoptive transfer. In the present report we extend this examination of insulin-specific T cells to lines and clones established from mice ranging in age from 4-12 weeks. These clones were found to be very similar to those from 7- and 12-week-old mice. The response was directed to the same peptide and most were found to produce IFN gamma, but none produced IL-4.
在NOD小鼠中积累的胰岛浸润物中，胰岛素特异性T细胞在名义上的胰岛细胞特异性T细胞中以高频率存在。在之前一份检查从7周龄和12周龄小鼠获得的克隆的报告中，我们鉴定出B链的一个15个氨基酸残基的肽段是这种反应的主要表位。尽管对胰岛素的反应似乎针对这一单一肽段，但观察到了不同的TCR Vβ使用情况。胰岛素特异性T细胞导致β细胞损伤这一点由以下事实表明：所有测试的克隆在过继转移后都能介导β细胞破坏。在本报告中，我们将对胰岛素特异性T细胞的检查扩展到从4至12周龄小鼠建立的细胞系和克隆。发现这些克隆与来自7周龄和12周龄小鼠的克隆非常相似。反应针对相同的肽段，并且大多数被发现产生IFNγ，但没有一个产生IL-4。
