Analysis of adaptive expression of a T cell self-recognizing structure in radiation bone marrow chimeras.

针对i区控制表位的单克隆抗体（mAb）仅在成熟的功能性T细胞上表达，而在B细胞和巨噬细胞上不表达（抗iat和抗i- j），被发现可以抑制免疫回路中II类mhc限制性细胞相互作用。本研究旨在分析Iat和I-J表位在T细胞上的表达机制，并研究这些分子在免疫调节中的功能作用。获得了四个重要发现：首先，Iat/I-J表位根据辐射骨髓嵌合体的环境MHC发生系统性改变。其次，I-J表位不是T细胞抗原受体（TcR）的独特型决定因子，而是位于与TcR不同的分子上。第三，我们已经能够通过特异性免疫沉淀来鉴定克隆T细胞的I-J分子。检测到的I-J分子是由45K糖肽亚基组成的90K二聚体分子，与TcR或CD28不同。最后，I-J分子与特异性mAb交联，抑制抗原和MHC特异性刺激诱导的Ca_<++>内流。这些结果表明，I-J（可能也包括Iat）是T细胞表面的一种分子，它通过TcR/T3复合物介导的T细胞活化的胞内信使的水解来传递信号。

Monoclonal antibodies (mAb) against I-region-controlled epitopes expressed exclusively on mature functional T cells but not on B cells and macrophages (anti-Iat and anti-I-J) were found to inhibit class II MHC-restricted cell interactions in the immunological circuit. The present study was undertaken to analyze a mechanism of expression of Iat and I-J epitopes on T cells and to study a functional role of these molecules in immune regulation. Four essential findings were obtained: first, Iat/I-J epitopes undergo systematic alterations according to the environmental MHC in radiation bone marrow chimeras. Secondary, the I-J epitope is not an idiotypic determinant of T cell antigen-receptor (TcR) but is on a distinct molecule from TcR. Third, we have been able to identify the I-J molecule of cloned T cells by the specific immunoprecipitation. The I-J molecule detected is a 90K dimeric molecule composed of 45K glycopeptide subunits distinct from TcR or CD28. Finally, the cross-linking of I-J molecules with specific mAb resulted in the inhibition of Ca_<++> influx induced via the specific stimulation by antigen and MHC. These results indicated that I-J (probably Iat as well) is a T cell surface molecule that transduces a signal to regulate the hydrolysis of intracellular messengers of T cell activation induced via the TcR/T3 complex.