Waksal S D, Borel Y
J Immunol. 1980 Mar;124(3):1506-9.
Hapten-conjugated isologous mouse gamma-globulin (TNP-MGG) can induce specific unresponsiveness in spleen populations for primary antibody responses in vitro to both T-dependent (TNP-KLH) and T-independent (TNP-LPS) antigens. This was also tested simultaneously for its influence on spleen populations in the generation of cytotoxic effector cell populations to hapten-modified self. Unlike its effect on primary antibody responses (tolerogenic), TNP-MGG does not inhibit the generation of cytotoxic T cells against TNBS-treated syngeneic spleen cells. TNP-MGG was also unable to act as an immunogen in generating cytotoxic effectors against TNBS-treated spleen cells. These data show that although TNP-MGG has a tolerogenic effect on B lymphocytes (and possibly helper T lymphocytes) it does not block the generation of killer T lymphocytes directed against the hapten-modified spleen cells. A different mechanism of tolerance induction for TNP-MGG compared to hapten-modified syngeneic murine spleen is therefore suggested.
半抗原结合的同源小鼠γ球蛋白(TNP-MGG)可在体外诱导脾细胞群体对T依赖性(TNP-KLH)和T非依赖性(TNP-LPS)抗原的初次抗体应答产生特异性无反应性。同时还检测了其对脾细胞群体产生针对半抗原修饰自身的细胞毒性效应细胞群体的影响。与它对初次抗体应答的作用(致耐受性)不同,TNP-MGG并不抑制针对经TNBS处理的同基因脾细胞的细胞毒性T细胞的产生。TNP-MGG也不能作为免疫原产生针对经TNBS处理的脾细胞的细胞毒性效应细胞。这些数据表明,尽管TNP-MGG对B淋巴细胞(可能还有辅助性T淋巴细胞)有致耐受性作用,但它并不阻断针对半抗原修饰脾细胞的杀伤性T淋巴细胞的产生。因此提示TNP-MGG与半抗原修饰的同基因小鼠脾脏相比,其诱导耐受性的机制不同。