Perry L L, Greene M I
Fed Proc. 1981 Jan;40(1):39-44.
Suppressor T cell (Ts) regulation of immunity to chemically induced syngeneic tumors has been investigated with regard to the mechanism of Ts stimulation and cell-to-cell communication. It has been determined that suppressor cells generated by the presence of tumor antigen participate in a suppressive circuit involving both cells and cell-derived factor(s) in the expression of suppressive effects. Evidence is provided that these interactions occur via idiotype--antiidiotype recognition in a manner similar to those in hapten-specific immune response. Conditions for induction of Ts activity in vivo have been artificially created by a variety of means, including the intravenous administration of soluble antigen and the inhibition of antigen-presenting function by anti-I-A antibodies or by in vivo treatment with ultraviolet irradiation. Suppression appears to be directed against the Ly-1+ cell, which mediates tumor immunity in this system. The summary of evidence suggest that responses to tumor antigen are in many aspects analogous to those occurring in response to more conventional antigens, but are subject to the dampening effects of suppressor cells generated continually during the period of primary tumor growth.
针对抑制性T细胞(Ts)对化学诱导的同基因肿瘤免疫的调节作用,已就Ts刺激机制和细胞间通讯进行了研究。已确定,肿瘤抗原的存在所产生的抑制细胞参与了一个抑制回路,该回路在抑制作用的表达中涉及细胞和细胞衍生因子。有证据表明,这些相互作用通过独特型-抗独特型识别发生,其方式类似于对半抗原特异性免疫反应中的相互作用。已通过多种手段人为创造了体内诱导Ts活性的条件,包括静脉内给予可溶性抗原以及用抗I-A抗体抑制抗原呈递功能或通过紫外线照射进行体内治疗。抑制作用似乎针对Ly-1+细胞,该细胞在此系统中介导肿瘤免疫。证据总结表明,对肿瘤抗原的反应在许多方面类似于对更传统抗原的反应,但受到原发性肿瘤生长期间持续产生的抑制细胞的抑制作用。