Sumida T, Takei I, Taniguchi M
J Immunol. 1984 Sep;133(3):1131-6.
The molecular mechanisms of activation of immunoregulatory T cells were characterized by using two complementary suppressor T cell hybridoma systems: the KLH-specific monoclonal suppressor factor (KLH-TsF), and the inducible acceptor-suppressor hybridoma line with anti-idiotypic receptor for KLH-TsF. It was demonstrated that the identity of the KLH specificity and genetic specificity was required for the TsF-acceptor interaction. These specificities were found to be mediated by the two polypeptide chains of TsF: KLH-binding, Ct-bearing heavy chain and I-J+ light chain. These two chains were essential for stimulation of the acceptor hybridoma. The results were also confirmed by the findings that the mixture of the 11S and 13S mRNA translation products reconstituted the active TsF to stimulate the acceptor hybridoma. Furthermore, the genetic restriction observed was found to be mediated by the I-J+ light chain and to be governed by the gene linked to the H-2 complex but not to the Igh genes. The gene controlling the restriction specificity was strongly suggested to be in the intra-H-2 complex, but not outside of the H-2 complex.
通过使用两种互补的抑制性T细胞杂交瘤系统来表征免疫调节性T细胞激活的分子机制:钥孔戚血蓝蛋白特异性单克隆抑制因子(KLH-TsF),以及具有针对KLH-TsF的抗独特型受体的诱导型受体-抑制杂交瘤系。结果表明,TsF-受体相互作用需要KLH特异性和遗传特异性的一致性。发现这些特异性由TsF的两条多肽链介导:结合KLH的、携带Ct的重链和I-J⁺轻链。这两条链对于刺激受体杂交瘤至关重要。11S和13S mRNA翻译产物的混合物可重构活性TsF以刺激受体杂交瘤,这一发现也证实了上述结果。此外,观察到的遗传限制由I-J⁺轻链介导,并由与H-2复合体相关但与Igh基因无关的基因控制。强烈提示控制限制特异性的基因位于H-2复合体内,而非H-2复合体之外。