McDuffie M, Schweiger D, Reitz B, Ostrowska A, Knight A M, Dyson P J
Barbara Davis Center for Childhood Diabetes, University of Colorado Health Sciences Center, Denver 80262.
J Immunol. 1992 Apr 1;148(7):2097-102.
Analysis of TCR beta-chain V region (V beta) frequency among NOD lymphocytes reveals a profound depletion of V beta 3+ T cells, and a recent study has linked this phenomenon to the Mtv-3 insertion on chromosome 11. When the V beta 17a gene segment is introduced into mice with an nonobese diabetic mouse background, T cells bearing the TCR encoded by this gene segment are also dramatically reduced in frequency. Deletion of V beta 17a+ T cells segregates with deletion of T cells bearing V beta 3 and occurs in the absence of I-E, which had been shown in previous studies to be a major deleting element for V beta 17a+ thymocytes.
对非肥胖糖尿病（NOD）淋巴细胞中T细胞受体β链V区（Vβ）频率的分析显示，Vβ3 + T细胞显著减少，并且最近的一项研究将此现象与11号染色体上的Mtv - 3插入联系起来。当将Vβ17a基因片段导入具有非肥胖糖尿病小鼠背景的小鼠中时，携带由该基因片段编码的T细胞受体的T细胞频率也显著降低。Vβ17a + T细胞的缺失与携带Vβ3的T细胞的缺失相关，并且在没有I - E的情况下发生，先前的研究表明I - E是Vβ17a +胸腺细胞的主要删除元件。
