Klonowski Kimberly D, Williams Kristina J, Marzo Amanda L, Lefrançois Leo
Department of Immunology, Center for Integrative Immunology and Vaccine Research, University of Connecticut Health Center, 2634 Farmington Avenue, Farmington, CT 06030, USA.
J Immunol. 2006 Oct 1;177(7):4247-51. doi: 10.4049/jimmunol.177.7.4247.
Expression of IL-7Ralpha on a subset of Ag-specific effector CD8 T cells is believed to identify memory cell precursors. However, whether IL-7 regulates IL-7Ralpha expression in vivo and is responsible for selective survival of IL-7Ralpha(+) effector cells is unknown. Our results show that in the absence of IL-7, IL-7Ralpha expression was extinguished on the majority of CD8 T cells responding to virus infection, sustained on a subset of effector cells transitioning to memory, and expressed at high levels by memory cells. Additionally, an IL-7-deficient environment was capable of supporting bcl-2 up-regulation and memory cell development in response to virus infection. Thus, IL-7Ralpha regulation occurs independently of IL-7 in responding CD8 T cells, indicating that CD8 memory T cell precursors are not selected by IL-7/IL-7Ralpha interactions.
人们认为,在一部分抗原特异性效应性CD8 T细胞上白细胞介素-7受体α(IL-7Rα)的表达可识别记忆细胞前体。然而,IL-7是否在体内调节IL-7Rα的表达并负责IL-7Rα(+)效应细胞的选择性存活尚不清楚。我们的结果表明,在缺乏IL-7的情况下,对病毒感染作出反应的大多数CD8 T细胞上的IL-7Rα表达消失,在一部分向记忆细胞转变的效应细胞上持续存在,并在记忆细胞中高水平表达。此外,IL-7缺陷环境能够支持病毒感染后bcl-2上调和记忆细胞发育。因此,在反应性CD8 T细胞中,IL-7Rα的调节独立于IL-7发生,这表明CD8记忆T细胞前体不是通过IL-7/IL-7Rα相互作用选择的。