| First Author | Tang J | Year | 2015 |
| Journal | Int Immunopharmacol | Volume | 28 |
| Issue | 2 | Pages | 931-7 |
| PubMed ID | 25864622 | Mgi Jnum | J:318303 |
| Mgi Id | MGI:6859132 | Doi | 10.1016/j.intimp.2015.03.036 |
| Citation | Tang J, et al. (2015) IL-25 promotes the function of CD4+CD25+ T regulatory cells and prolongs skin-graft survival in murine models. Int Immunopharmacol 28(2):931-7 |
| abstractText | Interleukin (IL)-25, also known as IL-17E, belongs to the IL-17 family of cytokines. Unlike other IL-17 family members, IL-25 promotes Th2-type immune responses, stimulating IL-4, IL-5, and IL-13 production. Here, we employed murine models of skin graft to explore the role of IL-25 in suppression of graft rejection. We found that IL-25 expression is increased during allograft rejection, and allograft rejection was enhanced in IL-25 KO mice. IL-25 KO was associated with down-regulation of Foxp3 expression in CD4+ T cells. Further, while adoptive transfer of WT regulatory T cells (Tregs) protected against allograft rejection, adoptive transfer of IL-25 deficient Tregs failed to protect against allograft rejection. Exogenous IL-25 restored Foxp3 expression and Treg function in vitro. Moreover, IL-25 promoted phosphorylation of NFAT2. Thus, IL-25 may enhance Treg function by up-regulating NFAT2 phosphorylation. Our findings suggest that IL-25 can sustain Foxp3 expression, enhance the suppressive function of Tregs, and prolong skin-graft survival. |
