Molecular Basis for the Immune Regulatory Receptor System

配对的免疫球蛋白样受体(PIR-B)是一种基于酪氨酸的MHC-I类分子抑制受体，可能参与B-1细胞的调节，因为B-1细胞中PIR-B的表达是B-2细胞或常规B细胞的数倍。最近意想不到的发现表明，PIR-B通过与包括Nogo在内的三种髓鞘轴突生长抑制剂结合，在轴突再生中发挥了新的抑制作用。因此，就PIR-B介导的免疫和神经细胞抑制而言，确定抑制髓鞘蛋白和MHCI的作用是否可以共存或相互排斥变得有趣。我们对这个问题进行了研究，并获得了支持Nogo和MHCI介导的抑制共存的数据。我们现在提出了一种新的机制，PIR-B介导的调节是通过免疫系统细胞中的MHCI和Nogo双重实现的。

Paired immunoglobulin-like receptor (PIR)-B, an immunoreceptor tyrosine-based inhibitory motif-harboring receptor for MHC class I molecules, could participate in the regulation of B-1 cells, because PIR-B expression is several times higher in B-1 cells than in B-2 cells or conventional B cells. Recent unexpected findings pointed to a novel inhibitory role of PIR-B in neurite regeneration through binding to three axonal outgrowth inhibitors of myelin including Nogo. Thus, it becomes interesting to determine whether the actions of the inhibitory myelin proteins and MHCI could coexist or be mutually exclusive as to the PIR-B-mediated immune and neural cell inhibition. We studied this subject and obtained data supporting the coexistence of Nogo- and MHCI-mediated inhibition. We now propose a novel mechanism by which PIR-B-mediated regulation is achieved dually via MHCI and Nogo in cells of the immune system.