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首页> 美国卫生研究院文献>The Journal of Experimental Medicine >IL-31–IL-31R interactions negatively regulate type 2 inflammation in the lung
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IL-31–IL-31R interactions negatively regulate type 2 inflammation in the lung

机译：IL-31–IL-31R相互作用负面调节肺中的2型炎症

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摘要

Interleukin (IL) 31Rα (glycoprotein 130–like monocyte receptor and glycoprotein 130–like receptor) heterodimerizes with oncostatin M receptor β to bind IL-31, a cytokine expressed preferentially by CD4+ T helper type 2 (Th2) cells. However, the functions of IL-31–IL-31R signaling in immune regulation remain unknown. Here, we identify a novel role for IL-31R in limiting type 2 inflammation in the lung. After intravenous injection of Schistosoma mansoni eggs, IL-31Rα−/− mice developed severe pulmonary inflammation, characterized by an increase in the area of granulomatous inflammation, increased numbers of resistin-like molecule α+ cells, and enhanced collagen deposition compared to WT counterparts. In vitro, macrophages generated from IL-31Rα−/− mice promoted enhanced ovalbumin-specific CD4+ T cell proliferation and purified naive CD4+ T cells from IL-31Rα−/− mice exhibited enhanced proliferation and expression of Th2 cytokines, identifying a T cell– and macrophage-intrinsic regulatory function for IL-31R signaling. In contrast, the generation of CD4+ T cell–mediated Th1 responses were normal in IL-31Rα−/− mice, suggesting that the regulatory role of IL-31R signaling is limited to type 2 responses. Together, these data implicate IL-31R signaling as a novel negative regulatory pathway that specifically limits type 2 inflammation.
机译：白介素（IL）31Rα（糖蛋白130样单核细胞受体和糖蛋白130样受体）与制瘤素M受体β异源二聚体结合IL-31，IL-31是一种优先由CD4 + 2型辅助细胞表达的细胞因子（ Th2）细胞。但是，IL-31–IL-31R信号在免疫调节中的功能仍然未知。在这里，我们确定IL-31R在限制肺部2型炎症中的新作用。静脉注射曼氏血吸虫卵后，IL-31Rα-/-小鼠出现严重的肺部炎症，其特征是肉芽肿性炎症区域增加，抵抗素样分子α +数量增加细胞，与WT相比，胶原沉积增强。在体外，由IL-31Rα-/-小鼠产生的巨噬细胞可促进卵清蛋白特异性CD4 + T细胞增殖并纯化纯净的CD4 + T IL-31Rα-/-小鼠的细胞显示出增强的Th2细胞因子增殖和表达，从而鉴定了IL-31R信号的T细胞和巨噬细胞内在调节功能。相反，在IL-31Rα-/-小鼠中，CD4 + T细胞介导的Th1应答的生成是正常的，这表明IL-31R信号的调节作用是仅限于类型2的响应。总之，这些数据暗示IL-31R信号传导是特异性限制2型炎症的新型负调控途径。

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