Division of Rheumatology, Department of Internal Medicine, University of Geneva School of Medicine, Switzerland.
Blood. 2012 Oct 25;120(17):3478-87. doi: 10.1182/blood-2012-06-439026. Epub 2012 Sep 11.
The interleukin-1 (IL-1) superfamily of cytokines comprises a set of pivotal mediators of inflammation. Among them, the action of IL-36 cytokines in immune responses has remained elusive. In a recent study, we demonstrated a direct effect of IL-36 on immune cells. Here we show that, among T cells, the IL-36 receptor is predominantly expressed on naive CD4(+) T cells and that IL-36 cytokines act directly on naive T cells by enhancing both cell proliferation and IL-2 secretion. IL-36β acts in synergy with IL-12 to promote Th1 polarization and IL-36 signaling is also involved in mediating Th1 immune responses to Bacillus Calmette-Guerin infection in vivo. Our findings point toward a critical function of IL-36 in the priming of Th1 cell responses in vitro, and in adaptive immunity in a model of mycobacterial infection in vivo.
白细胞介素-1 (IL-1) 细胞因子超家族包括一组炎症的关键介质。在这些细胞因子中，IL-36 细胞因子在免疫反应中的作用仍不明确。在最近的一项研究中，我们证明了 IL-36 对免疫细胞的直接作用。在这里，我们表明在 T 细胞中，IL-36 受体主要表达在幼稚 CD4(+) T 细胞上，IL-36 细胞因子通过增强细胞增殖和 IL-2 分泌直接作用于幼稚 T 细胞。IL-36β 与 IL-12 协同作用促进 Th1 极化，IL-36 信号也参与介导卡介苗感染体内 Th1 免疫反应。我们的研究结果表明，IL-36 在体外 Th1 细胞反应的启动以及体内分枝杆菌感染模型中的适应性免疫中具有关键功能。
