The Beirne B. Carter Center for Immunology Research, The University of Virginia, Charlottesville, Virginia, USA.
Nat Immunol. 2011 Apr;12(4):327-34. doi: 10.1038/ni.1996. Epub 2011 Feb 6.
Interleukin (IL)-10 is an important regulatory cytokine that can modulate excessive immune mediated injury. Several distinct cell types have been demonstrated to produce IL-10, including most recently CD8+ cytotoxic T lymphocytes (CTLs) responding to respiratory virus infection. Here we report that CD4+ T cell help in the form of IL-2 is required for IL-10 production by CTLs, but not for the induction of CTL effector cytokines. We show that IL-2 derived from CD4+ helper T cells cooperates with innate immune cell-derived IL-27 to amplify IL-10 production by CTLs through a Blimp-1-dependent mechanism. These findings reveal a previously unrecognized pathway that coordinates signals derived from innate and helper T cells to control the production of a regulatory cytokine by CTLs during acute viral infection.
白细胞介素（IL）-10 是一种重要的调节性细胞因子，可调节过度的免疫介导损伤。已经证明几种不同的细胞类型可以产生 IL-10，包括最近对呼吸道病毒感染做出反应的 CD8+细胞毒性 T 淋巴细胞（CTL）。在这里，我们报告说，CTL 产生 IL-10 需要以 IL-2 形式存在的 CD4+T 细胞辅助，但不需要诱导 CTL 效应细胞因子。我们表明，来自 CD4+辅助 T 细胞的 IL-2 与先天免疫细胞衍生的 IL-27 合作，通过 Blimp-1 依赖性机制放大 CTL 产生的 IL-10。这些发现揭示了一个以前未被识别的途径，该途径协调来自先天和辅助 T 细胞的信号，以控制急性病毒感染期间 CTL 产生调节性细胞因子。
