Benjamin R J, Qin S X, Wise M P, Cobbold S P, Waldmann H
Department of Pathology, University of Cambridge, GB.
Eur J Immunol. 1988 Jul;18(7):1079-88. doi: 10.1002/eji.1830180717.
In vivo therapy with a CD4 (L3T4) monoclonal antibody is able to provide a tolerogenic milieu for a limited number of protein antigens. In this study we have analyzed the mechanisms of such tolerance to human gamma globulin, and show that tolerance is induced in adult T helper cells without a need for cellular depletion, and that it is probably not maintained by suppressor mechanisms nor by regulatory cellular circuits involving CD8+ (Ly-2+) cells. Tolerance induction is not a property peculiar to the CD4 molecule, as similar effects can be elicited with a monoclonal antibody directed to the CD11a (LFA-1) molecule. We suggest that tolerance is maintained by the functional deletion of mature T helper cells and that adhesion molecules, such as CD4, CD8 and CD11a, may play a critical role in T cell discernment of self from nonself.
用CD4（L3T4）单克隆抗体进行体内治疗能够为有限数量的蛋白质抗原提供一个致耐受性环境。在本研究中，我们分析了对人γ球蛋白产生这种耐受性的机制，结果表明，在成年T辅助细胞中可诱导产生耐受性，而无需细胞清除，并且这种耐受性可能不是由抑制机制或涉及CD8 +（Ly - 2 +）细胞的调节细胞回路维持的。耐受性诱导并非CD4分子所特有的特性，因为针对CD11a（LFA - 1）分子的单克隆抗体也能引发类似效应。我们认为，耐受性是通过成熟T辅助细胞的功能性缺失来维持的，并且诸如CD4、CD8和CD11a等黏附分子可能在T细胞区分自身与非自身方面发挥关键作用。
