Schuler W, Schuler A, Bosma M J
Fox Chase Cancer Center, Institute for Cancer Research, Philadelphia.
Eur J Immunol. 1990 Mar;20(3):545-50. doi: 10.1002/eji.1830200313.
The status of T cell receptor gamma chain genes (TcR gamma) in 11 spontaneous T cell lymphomas from mice with severe combined immune deficiency (scid) was analyzed. We found that as a result of large abnormal deletions accompanying attempted site-specific V-to-J recombinations, 36 of 47 rearranged TcR gamma genes lacked the variable (V) and/or joining (J) region gene segment involved in this attempted recombination. No such deletions were found in T cell lymphomas from normal mice. We interpret our data as indicating a defective V-to-J recombination in scid lymphocytes consistent with our earlier observation of faulty D-to-J recombination in transformed scid lymphocytes (Schuler et al., Cell 1986. 46: 963). The present results further support the hypothesis that the scid mutation affects a component of the VDJ-recombinase system used in common by B and T cells to assemble antigen receptor genes.
分析了严重联合免疫缺陷（scid）小鼠的11例自发性T细胞淋巴瘤中T细胞受体γ链基因（TcRγ）的状态。我们发现，由于伴随位点特异性V - J重排尝试出现大量异常缺失，47个重排的TcRγ基因中有36个缺少参与该重排尝试的可变（V）和/或连接（J）区域基因片段。在正常小鼠的T细胞淋巴瘤中未发现此类缺失。我们将数据解释为表明scid淋巴细胞中V - J重排存在缺陷，这与我们早期在转化的scid淋巴细胞中观察到的错误D - J重排一致（舒勒等人，《细胞》1986年。46:963）。目前的结果进一步支持了scid突变影响B细胞和T细胞共同用于组装抗原受体基因的VDJ重组酶系统的一个组分这一假说。
