O'Neill H C
Developmental Haematology Group, John Curtin School of Medical Research, Australian National University, Canberra.
Leukemia. 1991 Nov;5(11):921-7.
The 5C2 cell line was derived following culture of mouse spleen cells exposed in vivo and in vitro to radiation leukemia virus (RadLV) containing supernatants from the C6VL/1 T cell lymphoma. This cell line has been found to express an alpha beta T-cell receptor (TCR) identifiable with the Mab124-40 anti-clonotypic antibody which is specific for C6VL/1. It has been shown to be genetically and phenotypically distinct from C6VL/1 with a unique phenotype, i.e. CD4-, CD8-, CD3+, TCR-alpha beta. 5C2 has been shown to express high levels of alpha and beta chain mRNA and to utilize the same or similar V alpha and V beta region genes as C6VL/1. Whereas C6VL/1 binds cross-reactively to both RadLV/C6VL and an unrelated isolate RadLV/VL3, 5C2 has binding specificity for only RadLV/C6VL, which induced its proliferation. The anti-clonotypic antibody Mab124-40 specifically and completely inhibits binding of 5C2 to RadLV/C6VL at concentrations as low as 300 ng/ml. The 5C2 cell line can also be stimulated to increased proliferation by RadLV/C6VL. All of these data are consistent with the role of a TCR alpha beta heterodimer in binding and stimulation by RadLV and satisfy one prediction of the receptor-mediated leukemogenesis hypothesis that T-cell clones identifiable by their T-cell receptor clonotype may be targets for transformation by a particular retrovirus.
5C2细胞系是在体内和体外将小鼠脾细胞培养于含有来自C6VL/1 T细胞淋巴瘤的上清液的辐射白血病病毒(RadLV)后获得的。已发现该细胞系表达一种αβ T细胞受体(TCR),可用对C6VL/1特异的单克隆抗体Mab124 - 40鉴定。已证明它在遗传和表型上与C6VL/1不同,具有独特的表型,即CD4 - 、CD8 - 、CD3 + 、TCR - αβ。已证明5C2表达高水平的α和β链mRNA,并利用与C6VL/1相同或相似的Vα和Vβ区域基因。虽然C6VL/1与RadLV/C6VL和一种无关的分离株RadLV/VL3都有交叉反应性结合,但5C2仅对RadLV/C6VL有结合特异性,后者可诱导其增殖。抗克隆型抗体Mab124 - 40在低至300 ng/ml的浓度下能特异性且完全抑制5C2与RadLV/C6VL的结合。5C2细胞系也可被RadLV/C6VL刺激而增加增殖。所有这些数据都与TCRαβ异二聚体在RadLV结合和刺激中的作用一致,并满足受体介导的白血病发生假说的一个预测,即由其T细胞受体克隆型鉴定的T细胞克隆可能是特定逆转录病毒转化的靶标。