Weinberger J Z, Benacerraf B, Dorf M E
J Exp Med. 1980 Jun 1;151(6):1413-23. doi: 10.1084/jem.151.6.1413.
4-Hydroxy-3-nitrophenyl acetyl (NP)-derivatized syngeneic spleen cells administered intravenously induced a population of suppressor T cells that could suppress mice previously primed to NP. The effect was demonstrable when the suppressor cells were transferred to NP-primed mice on the day of challenge for delayed-type hypersensitivity (DTH) responses. In contrast to the suppressor T cell population, which abrogates 5-iodo derivative of NP (NIP)-specific DTH responses when administered before antigen priming, the effector-phase suppressors did not efficiently suppress NIP-specific DTH responses, and were not lysed by treatment with antiidiotype plus complement. Adoptive transfer experiments between major histocompatibility complex and allotype congenic strains of mice allowed demonstration of both Igh-V and I-A restrictions in the transfer of this cell population. The implications of these data in terms of network theories and proposed cellular models for negative immunoregulation were discussed.
静脉注射4-羟基-3-硝基苯乙酰(NP)衍生的同基因脾细胞可诱导出一群抑制性T细胞,这些细胞能够抑制先前已对NP致敏的小鼠。当在迟发型超敏反应(DTH)攻击当天将抑制性细胞转移到已用NP致敏的小鼠体内时,这种效应是可证实的。与在抗原致敏前给予时可消除NP的5-碘衍生物(NIP)特异性DTH反应的抑制性T细胞群体不同,效应期抑制细胞不能有效地抑制NIP特异性DTH反应,并且用抗独特型加补体处理后不会被裂解。在主要组织相容性复合体和小鼠同种异型同基因品系之间进行的过继转移实验表明,在这种细胞群体的转移中存在Igh-V和I-A限制。讨论了这些数据在网络理论和提出的负性免疫调节细胞模型方面的意义。