Hara M, Kitani A, Harigai M, Suzuki K, Hirose T, Kawakami M, Kawagae M, Nakamura H
1st Department of Internal Medicine, National Defence Medical College, Saitama, Japan.
Scand J Immunol. 1991 Feb;33(2):141-9. doi: 10.1111/j.1365-3083.1991.tb03744.x.
To investigate autologous antigen recognition, we developed two autoreactive CD4+ T-cell clones, A2 and A10, maintained with non-T cells and IL-2. Autologous non-T-cell stimulation of the T-cell clones resulted in a decrease in cell surface expression of CD4, whereas the expression of CD2, CD3, and WT31 was unchanged. Activation of the autoreactive T-cell clones by cell surface binding anti-CD3 MoAb, as a specific antigen stimulator of the T-cell receptor complex, induced cell surface antigen comodulation of CD3, CD4, and WT31. These data suggest a discrete association of CD3 and CD4 molecules in T-cell stimulation, acting through the autologous mixed lymphocyte reaction and the CD3/T-cell receptor complex. PMA treatment resulted in concomitant down-regulation of CD3 and CD4 but calcium ionophore treatment did not. Thus, it appears that phosphorylation of CD3 leads to the down-regulation of surface antigens of CD4.
为了研究自身抗原识别，我们构建了两个自身反应性CD4+ T细胞克隆A2和A10，并用非T细胞和白细胞介素-2进行培养。对T细胞克隆进行自身非T细胞刺激导致CD4细胞表面表达下降，而CD2、CD3和WT31的表达未发生变化。作为T细胞受体复合物的特异性抗原刺激剂，通过细胞表面结合抗CD3单克隆抗体激活自身反应性T细胞克隆，可诱导CD3、CD4和WT31的细胞表面抗原共调节。这些数据表明，在T细胞刺激过程中，CD3和CD4分子通过自身混合淋巴细胞反应和CD3/T细胞受体复合物存在离散关联。佛波酯（PMA）处理导致CD3和CD4同时下调，但钙离子载体处理则不会。因此，似乎CD3的磷酸化导致了CD4表面抗原的下调。
