Abstract
Abstract Interleukin (IL)-25, also known as Interleukin (IL)-17E, belonging to the IL-17 family. Unlike the other members, IL-25 has long been deemed as a pro-inflammatory cytokine favoring Th2--type immune response. Here, we show that expression of IL-25 in skin and subcutaneous tissues were constantly, while increased during allograft rejection. At same time, deficiency of IL-25 aggravates skin allograft rejection in murine models. Further experiments showed deficiency of IL-25 down-regulated the expression of Foxp3 among CD4+ cells and aggravated skin allograft rejections in murine models. While, exogenous IL-25 restored the Foxp3 expression and the function of Tregs in vitro. Adoptively transfer of IL-25 deficient Tregs failed to protect the allograft from rejection, compared to the WT Tregs. Moreover, IL-25 promoted phosphorylation of NFAT2, up-regulated the Foxp3 expression and contributed to the function of Tregs. Our findings indicate that IL-25 can promote the function of Tregs via impeding the interaction of NFAT2 and Foxp3, and prolong skin-graft survival.
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