Sad S, Kägi D, Mosmann T R
Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, Canada.
J Exp Med. 1996 Oct 1;184(4):1543-7. doi: 10.1084/jem.184.4.1543.
During an immune response, effector CD8+ T cells can kill infected cells by the perforin-dependent pathway. In comparison to CD4+ T cells, which are major sources of cytokines, normal CD8+ T cells produced less interleukin 2 and interferon gamma, and proliferated less vigorously after antigenic stimulation. Killing of target cells was a major cause of these reduced responses, since perforin-deficient CD8+ T cells showed substantially increased cytokine synthesis and proliferation. Cytotoxicity by the alternate Fas pathway also resulted in self-limitation of CD8+ T cell cytokine synthesis. This relationship between cytotoxicity and cytokine synthesis may regulate CD8+ T function in different phases of an immune response.
在免疫反应过程中,效应性CD8 + T细胞可通过穿孔素依赖性途径杀死受感染细胞。与作为细胞因子主要来源的CD4 + T细胞相比,正常CD8 + T细胞产生的白细胞介素2和干扰素γ较少,并且在抗原刺激后增殖能力较弱。靶细胞的杀伤是这些反应减弱的主要原因,因为缺乏穿孔素的CD8 + T细胞显示出细胞因子合成和增殖大幅增加。通过替代性Fas途径的细胞毒性也导致CD8 + T细胞细胞因子合成的自我限制。细胞毒性与细胞因子合成之间的这种关系可能在免疫反应的不同阶段调节CD8 + T细胞的功能。