Bikoff E K
J Exp Med. 1983 Dec 1;158(6):1868-80. doi: 10.1084/jem.158.6.1868.
Experiments presented in this report demonstrate that specificity of the Ly1+ T cell proliferative response to NP-modified Ig is controlled by Igh-C-linked genes. In addition, we describe the mechanism whereby Igh-C-encoded molecules influence Ly1+ T cell activity. We show that Igh-C-linked control of T cell responses to NP-modified Ig is a secondary consequence of naturally acquired tolerance for self Ig. Unresponsiveness to self Ig is not due to a defect expressed functionally at the level of the antigen-presenting cell, nor is it associated with active suppression. These results suggest that tolerance for self Ig at the level of the Ly1+ T cell is due to functional deletion of Ly1+ T cell clones specific for self Ig. The possibility is considered that regulatory effects mediated by passively administered antibodies may in part be due to induction of Ly1+ T cell tolerance for self Ig.
本报告中呈现的实验表明，Ly1⁺ T细胞对NP修饰的Ig的增殖反应特异性受Igh - C连锁基因控制。此外，我们描述了Igh - C编码分子影响Ly1⁺ T细胞活性的机制。我们表明，Igh - C对T细胞对NP修饰的Ig反应的控制是自然获得的自身Ig耐受性的次要结果。对自身Ig无反应性并非由于抗原呈递细胞水平上功能表达的缺陷，也与主动抑制无关。这些结果表明，Ly1⁺ T细胞水平上对自身Ig的耐受性是由于针对自身Ig的Ly1⁺ T细胞克隆的功能缺失。被动给予的抗体介导的调节作用部分可能是由于诱导Ly1⁺ T细胞对自身Ig的耐受性，这种可能性也被考虑在内。
