Tolerance for self IG at the level of the Ly1+ T cell.
Tolerance for self IG at the level of the Ly1+ T cell.
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Ly1 T 细胞水平对自身 IG 的耐受性。
DOI：
10.1084/jem.158.6.1868
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发表时间：
1983
期刊：
影响因子：
--
通讯作者：
Bikoff,EK
中科院分区：
文献类型：
--
作者：
Bikoff,EK
本报告中提出的实验表明，Ly1+ T 细胞对 NP 修饰 Ig 的增殖反应的特异性是由 Igh-C 连锁基因控制的。此外，我们描述了 Igh-C 编码分子影响 Ly1+ T 细胞活性的机制。我们发现，T 细胞对 NP 修饰的 Ig 反应的 Igh-C 连锁控制是自然获得的对自身 Ig 耐受的次要结果。对自身 Ig 无反应并不是由于抗原呈递细胞水平上功能性表达的缺陷，也与主动抑制无关。这些结果表明，Ly1+ T 细胞水平对自身 Ig 的耐受性是由于对自身 Ig 具有特异性的 Ly1+ T 细胞克隆的功能性缺失。人们认为，被动施用抗体介导的调节作用可能部分是由于诱导了 Ly1+ T 细胞对自身 Ig 的耐受。
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.