Department of Immunology, Genentech, South San Francisco, California, USA.
Nat Immunol. 2011 Oct 12;12(12):1159-66. doi: 10.1038/ni.2156.
Interleukin 17C (IL-17C) is a member of the IL-17 family that is selectively induced in epithelia by bacterial challenge and inflammatory stimuli. Here we show that IL-17C functioned in a unique autocrine manner, binding to a receptor complex consisting of the receptors IL-17RA and IL-17RE, which was preferentially expressed on tissue epithelial cells. IL-17C stimulated epithelial inflammatory responses, including the expression of proinflammatory cytokines, chemokines and antimicrobial peptides, which were similar to those induced by IL-17A and IL-17F. However, IL-17C was produced by distinct cellular sources, such as epithelial cells, in contrast to IL-17A, which was produced mainly by leukocytes, especially those of the T(H)17 subset of helper T cells. Whereas IL-17C promoted inflammation in an imiquimod-induced skin-inflammation model, it exerted protective functions in dextran sodium sulfate-induced colitis. Thus, IL-17C is an essential autocrine cytokine that regulates innate epithelial immune responses.
白细胞介素 17C（IL-17C）是白细胞介素 17 家族的成员，在细菌挑战和炎症刺激下选择性地在上皮细胞中诱导产生。在这里，我们表明 IL-17C 以独特的自分泌方式发挥作用，与由受体 IL-17RA 和 IL-17RE 组成的受体复合物结合，该受体复合物在上皮细胞组织中优先表达。IL-17C 刺激上皮炎症反应，包括促炎细胞因子、趋化因子和抗菌肽的表达，这与 IL-17A 和 IL-17F 诱导的反应相似。然而，IL-17C 是由不同的细胞来源产生的，如上皮细胞，而 IL-17A 主要由白细胞产生，特别是辅助性 T 细胞的 T(H)17 亚群。虽然 IL-17C 在咪喹莫特诱导的皮肤炎症模型中促进炎症，但它在葡聚糖硫酸钠诱导的结肠炎中发挥保护作用。因此，IL-17C 是一种重要的自分泌细胞因子，调节先天上皮免疫反应。
