Miller S D, Sy M S, Claman H N
J Immunol. 1978 Jul;121(1):274-80.
We investigated the mechanism(s) by which MHC-restricted suppressor T cells (Ts) induced by i.v. injection of allogeneic DNP-modified lymphoid cells (alloinduced Ts) suppress the DNFB contact sensitivity response. It was shown that alloinduced Ts acted only during the early phases (afferent limb) of sensitization. They were incapable of suppressing previously sensitized recipients or of inhibiting the expression of DNFB-immune LN cells when co-transferred into normal recipients. The target of alloinduced Ts seems to be cell proliferation, i.e., inhibition of antigen-induced cell proliferation (DNA synthesis) in Ts recipient mice. The failure of recipients of alloinduced Ts to generate DNFB-immune LN cells capable of transferring contact sensitivity to normal recipients also suggests that these Ts act by preventing the development of an expanded clone of mature immune T cells. The suppressive effects of alloinduced Ts also were inhibited by prior in vitro treatment with anti-TNP serum. The data are discussed in terms of current models of suppression, and are compared to mechanisms of suppression in other contact sensitivity models.
我们研究了静脉注射同种异体二硝基苯（DNP）修饰的淋巴细胞诱导的MHC限制抑制性T细胞（Ts）（同种异体诱导的Ts）抑制二硝基氟苯（DNFB）接触敏感性反应的机制。结果表明，同种异体诱导的Ts仅在致敏的早期阶段（传入支）起作用。当共同转移到正常受体中时，它们无法抑制先前致敏的受体，也无法抑制DNFB免疫淋巴结细胞的表达。同种异体诱导的Ts的靶标似乎是细胞增殖，即抑制Ts受体小鼠中抗原诱导的细胞增殖（DNA合成）。同种异体诱导的Ts的受体无法产生能够将接触敏感性转移给正常受体的DNFB免疫淋巴结细胞，这也表明这些Ts通过阻止成熟免疫T细胞扩增克隆的发育而起作用。同种异体诱导的Ts的抑制作用也被抗TNP血清的预先体外处理所抑制。根据当前的抑制模型对数据进行了讨论，并与其他接触敏感性模型中的抑制机制进行了比较。
