Ikezawa Z, Nonaka M, Abe R, Tada T, Nagy Z A, Klein J
J Immunol. 1983 Oct;131(4):1646-9.
Mouse strains carrying the kappa allele at loci A beta, A alpha, E beta, and E alpha are nonresponders to lactate dehydrogenase B (LDHB) and to allotypic determinants of IgG2a myeloma proteins (for example, UPC10 used in this study). The nonresponsiveness to these antigens is caused by T suppressor (Ts) cells that prevent antigen-primed T helper (Th) cells from proliferating. We demonstrate here that monoclonal antibodies specific for an A region-controlled molecule selectively expressed on T cells (A-T) are capable of inducing anti-LDHB and anti-UPC10 responses of primed T cells from nonresponder strains. A monoclonal anti-J antibody that cross-reacts with the A-T molecule also induces responsiveness, whereas another J-specific antibody that lacks this cross-reactivity fails to do so. The mechanism of response induction is blocking of the interaction between the Ts cell or its factor (TsF) and the target of suppression, the antigen-specific Lyt-1+2- (Th) cell. The blocking occurs at the level of the Ts cell and the TsF. The data indicate that Ts cells and TsF carry a unique, A region-controlled molecule that is not only functionally analogous but also serologically similar to the J molecule.
在β链、α链、Eβ链和Eα链基因座携带κ等位基因的小鼠品系对乳酸脱氢酶B(LDHB)和IgG2a骨髓瘤蛋白的同种异型决定簇(例如本研究中使用的UPC10)无反应。对这些抗原的无反应性是由抑制性T细胞(Ts)引起的,这些细胞会阻止抗原致敏的辅助性T细胞(Th)增殖。我们在此证明,对T细胞上选择性表达的A区域控制分子(A-T)具有特异性的单克隆抗体能够诱导无反应性品系中致敏T细胞产生抗LDHB和抗UPC10反应。与A-T分子发生交叉反应的单克隆抗J抗体也能诱导反应性,而另一种缺乏这种交叉反应性的J特异性抗体则不能。反应诱导的机制是阻断Ts细胞或其因子(TsF)与抑制靶点即抗原特异性Lyt-1+2-(Th)细胞之间的相互作用。这种阻断发生在Ts细胞和TsF水平。数据表明,Ts细胞和TsF携带一种独特的、A区域控制的分子,该分子不仅在功能上类似,而且在血清学上也与J分子相似。