Kyoizumi S, Akiyama M, Hirai Y, Kusunoki Y, Tanabe K, Umeki S
Department of Radiobiology, Radiation Effects Research Foundation, Hiroshima, Japan.
J Exp Med. 1990 Jun 1;171(6):1981-99. doi: 10.1084/jem.171.6.1981.
The TCR/CD3 complex plays a central role in antigen recognition and activation of mature T cells, and, therefore, abnormalities in the expression of the complex should induce unresponsiveness of T cells to antigen stimulus. Using flow cytometry, we detected and enumerated variant cells with loss or alteration of the surface TCR/CD3 expression among human mature CD4+ T cells. The presence of variant CD4+ T cells was demonstrated by isolating and cloning them from peripheral blood, and their abnormalities can be accounted for by alterations in TCR expression such as defects of protein expression and partial protein deletion. The variant frequency in peripheral blood increased with aging in normal donors and was highly elevated in patients with ataxia telangiectasia, an autosomal recessive inherited disease with defective DNA repair and variable T cell immunodeficiency. These findings suggest that such alterations in TCR expression are induced by somatic mutagenesis of TCR genes and can be important factors related to age-dependent and genetic disease-associated T cell dysfunction.
TCR/CD3复合物在成熟T细胞的抗原识别和激活过程中发挥核心作用,因此,该复合物表达异常应会导致T细胞对抗原刺激无反应。我们运用流式细胞术,在人类成熟CD4+ T细胞中检测并计数了表面TCR/CD3表达缺失或改变的变异细胞。通过从外周血中分离并克隆变异CD4+ T细胞,证实了其存在,且它们的异常可归因于TCR表达的改变,如蛋白质表达缺陷和部分蛋白质缺失。正常供体外周血中的变异频率随年龄增长而增加,而在共济失调毛细血管扩张症患者中则显著升高,这是一种常染色体隐性遗传病,伴有DNA修复缺陷和可变的T细胞免疫缺陷。这些发现表明,TCR表达的此类改变是由TCR基因的体细胞突变诱导的,并且可能是与年龄相关和遗传疾病相关的T细胞功能障碍的重要因素。