Both NLRP3 inflammasome and Th17 cells play important roles in the pathogenesis of systemic lupus erythematosus (SLE). Here we tried to investigate whether leptin promotes the differentiation of Th17 cells from lupus mice by activating the NLRP3 inflammasome. Th17 cells induced from MRL/Mp-Fas lpr mice splenocytes under Th17 polarizing condition were treated with leptin at scalar doses during the last 18 h of culture. The mRNA levels of IL-17A, IL-17F, RORγt, IL-1β, IL-18, NLRP3, ASC, and IL-1R1 were detected by quantitative PCR. IL-17A, IL-17F, IL-1β, and IL-18 were tested by ELISA, while the activity of caspase-1 and number of Th17 cells were counted by flow cytometry before/after inhibition of the NLRP3 inflammasome. We found that leptin pushed up the expression of IL-17A, IL-17F, NLRP3, and IL-1β and increased the number of Th17 cells in lupus mice, while the expression of IL-17A, RORγt, and IL-1β and the number of Th17 cells were decreased after inhibition of the NLRP3 inflammasome. Leptin promoted the differentiation of Th17 cells from lupus mice by activating the NLRP3 inflammasome.

中文翻译：

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瘦素通过激活NLRP3炎性小体促进从MRL / Mp-Fas lpr狼疮小鼠中Th17细胞的分化。

NLRP3炎性小体和Th17细胞在系统性红斑狼疮（SLE）的发病机理中均起重要作用。在这里，我们试图研究瘦素是否通过激活NLRP3炎性小体来促进狼疮小鼠Th17细胞的分化。在培养的最后18小时内，将瘦素以标量剂量处理在Th17极化条件下从MRL / Mp-Fas lpr小鼠脾细胞诱导的Th17细胞。通过定量PCR检测IL-17A，IL-17F，RORγt，IL-1β，IL-18，NLRP3，ASC和IL-1R1的mRNA水平。通过ELISA测试IL-17A，IL-17F，IL-1β和IL-18，而在抑制NLRP3炎性体之前/之后通过流式细胞术计数caspase-1的活性和Th17细胞的数目。我们发现瘦素可上调IL-17A，IL-17F，NLRP3的表达，NLRP3炎性体抑制后，狼疮小鼠IL-1和IL-1β的表达增加，Th17细胞的数目增加，IL-17A，RORγt和IL-1β的表达和Th17细胞的数目减少。瘦素通过激活NLRP3炎性小体促进狼疮小鼠Th17细胞的分化。