Zhang X, Sun S, Hwang I, Tough D F, Sprent J
Department of Immunology, IMM4, The Scripps Research Institute, La Jolla, California 92037, USA.
Immunity. 1998 May;8(5):591-9. doi: 10.1016/s1074-7613(00)80564-6.
Proliferation of memory-phenotype (CD44hi) CD8+ cells induced by infectious agents can be mimicked by injection of type I interferon (IFN I) and by IFN I-inducing agents such as lipopolysaccharide and Poly I:C; such proliferation does not affect naive T cells and appears to be TCR independent. Since IFN I inhibits proliferation in vitro, IFN I-induced proliferation of CD8+ cells in vivo presumably occurs indirectly through production of secondary cytokines, e.g., interleukin-2 (IL-2) or IL-15. We show here that, unlike IL-2, IL-15 closely mimics the effects of IFN I in causing strong and selective stimulation of memory-phenotype CD44hi CD8+ (but not CD4+) cells in vivo; similar specificity applies to purified T cells in vitro and correlates with much higher expression of IL-2Rbeta on CD8+ cells than on CD4+ cells.
感染因子诱导的记忆表型(CD44高表达)CD8⁺细胞增殖,可通过注射I型干扰素(IFN I)以及IFN I诱导剂(如脂多糖和聚肌胞苷酸)来模拟;这种增殖不影响初始T细胞,且似乎不依赖T细胞受体。由于IFN I在体外抑制增殖,因此IFN I在体内诱导的CD8⁺细胞增殖可能是通过次级细胞因子(如白细胞介素-2(IL-2)或IL-15)的产生间接发生的。我们在此表明,与IL-2不同,IL-15在体内引起对记忆表型CD44高表达CD8⁺(而非CD4⁺)细胞的强烈且选择性刺激方面,紧密模拟了IFN I的作用;类似的特异性在体外纯化的T细胞中也适用,并且与CD8⁺细胞上IL-2Rβ的表达远高于CD4⁺细胞相关。