抗体诱导的CD3/T细胞受体复合物调节通过抑制T细胞活化所涉及的早期代谢步骤导致T细胞不应答。
Antibody-induced modulation of the CD3/T cell receptor complex causes T cell refractoriness by inhibiting the early metabolic steps involved in T cell activation.
作者信息
Pantaleo G, Olive D, Poggi A, Pozzan T, Moretta L, Moretta A
出版信息
J Exp Med. 1987 Aug 1;166(2):619-24. doi: 10.1084/jem.166.2.619.
Abstract
We investigated the mechanism involved in T cell unresponsiveness that follows the monoclonal antibody-induced surface modulation of the CD3-TCR complex. We determined whether modulation of CD3-TCR affected the early metabolic steps such as [Ca2+]i rise and InsP3 formation. A strong inhibition of the increase on [Ca2+]i mediated by either anti-TCR or anti-CD2 mAbs was detected. In contrast, surface modulation of CD2 molecules did not prevent the [Ca2+]i increase induced by anti-TCR mAb. Similarly, InsP3 increase was strongly reduced only after modulation of CD3-TCR complex (but not of CD2 molecules). Therefore, it appears that surface modulation of CD3-TCR complex causes T cell refractoriness by inhibiting the very early metabolic events that follow receptor-ligand interactions.
摘要
我们研究了单克隆抗体诱导的CD3-TCR复合物表面调节后T细胞无反应性所涉及的机制。我们确定了CD3-TCR的调节是否影响早期代谢步骤，如[Ca2+]i升高和肌醇三磷酸（InsP3）形成。检测到抗TCR或抗CD2单克隆抗体介导的[Ca2+]i升高受到强烈抑制。相比之下，CD2分子的表面调节并不能阻止抗TCR单克隆抗体诱导的[Ca2+]i升高。同样，只有在CD3-TCR复合物（而非CD2分子）调节后，InsP3升高才会大幅降低。因此，似乎CD3-TCR复合物的表面调节通过抑制受体-配体相互作用后的早期代谢事件导致T细胞不应答。
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