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，但在B细胞和巨噬细胞上不表达（抗Iat和抗I-J），可抑制免疫回路中II类MHC限制性细胞相互作用。本研究分析了T细胞上Iat和I-J表位的表达机制，并研究了这些分子在免疫调节中的功能作用。获得了四个基本的发现：第一，Iat/I-J表位进行系统的改变，根据环境的MHC在辐射骨髓嵌合体。其次，I-J表位不是T细胞抗原受体（TcR）的独特型决定簇，而是在与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分子是由不同于TcR或CD 28的45 K糖肽亚基组成的90 K二聚体分子。最后，I-J分子与特异性mAb交联后，可抑制抗原和MHC特异性刺激诱导的Ca_（++）内流。这些结果表明，I-J（也可能是Iat）是T细胞表面分子，其转导信号以调节通过TcR/T3复合物诱导的T细胞活化的细胞内信使的水解。

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.