Kubo M, Sano K, Fujisawa I, Asano Y, Tada T
Department of Immunology, Faculty of Medicine, University of Tokyo.
Jpn J Cancer Res. 1989 Nov;80(11):1106-12. doi: 10.1111/j.1349-7006.1989.tb02266.x.
The immunization of C3H mice with irradiated syngeneic MM48 tumor cells induced specific tumor-neutralizing cells (TNC). The TNC activity was mediated by the L3T4+, Ly-2- T cell population, and the generation of TNC coincided with the appearance of delayed-type hypersensitivity response against MM48 antigen. The administration of an auto-I-Ak reactive T helper cell clone MS202 to normal C3H mice resulted in the facilitation of growth of MM48 tumor due to the induction of T suppressor (Ts) cells. Splenic T cells from animals given this T cell clone inhibited the TNC activity of immunized mice resulting in the escape of MM48 from the TNC effect. The surface phenotype of the Ts cells was L3T4+, Ly-2-. The Ts cells induced by the clone MS202 were totally antigen-nonspecific, and were able to suppress both the effector and inductive processes of TNC. The results suggest the presence of a physiological MHC-restricted T cell circuit that regulates immune responses against the growing tumors.
用经辐射的同基因MM48肿瘤细胞免疫C3H小鼠可诱导出特异性肿瘤中和细胞(TNC)。TNC活性由L3T4⁺、Ly-2⁻ T细胞群体介导,TNC的产生与针对MM48抗原的迟发型超敏反应的出现相一致。将自身I-Ak反应性T辅助细胞克隆MS202给予正常C3H小鼠,由于诱导了T抑制(Ts)细胞,导致MM48肿瘤生长加速。给予该T细胞克隆的动物的脾T细胞抑制了免疫小鼠的TNC活性,导致MM48逃脱TNC效应。Ts细胞的表面表型为L3T4⁺、Ly-2⁻。克隆MS202诱导的Ts细胞完全是非抗原特异性的,并且能够抑制TNC的效应和诱导过程。结果表明存在一种生理性的MHC限制性T细胞回路,其调节针对生长肿瘤的免疫反应。