| First Author | Cai Y | Year | 2011 |
| Journal | Immunity | Volume | 35 |
| Issue | 4 | Pages | 596-610 |
| PubMed ID | 21982596 | Mgi Jnum | J:177652 |
| Mgi Id | MGI:5295792 | Doi | 10.1016/j.immuni.2011.08.001 |
| Citation | Cai Y, et al. (2011) Pivotal Role of Dermal IL-17-Producing gammadelta T Cells in Skin Inflammation. Immunity 35(4):596-610 |
| abstractText | Interleukin-23 (IL-23) and CD4(+) T helper 17 (Th17) cells are thought to be critical in psoriasis pathogenesis. Here, we report that IL-23 predominantly stimulated dermal gammadelta T cells to produce IL-17 that led to disease progression. Dermal gammadelta T cells constitutively expressed the IL-23 receptor (IL-23R) and transcriptional factor RORgammat. IL-17 production from dermal gammadelta T cells was independent of alphabeta T cells. The epidermal hyperplasia and inflammation induced by IL-23 were significantly decreased in T cell receptor delta-deficient (Tcrd(-/-)) and IL-17 receptor-deficient (Il17ra(-/-)) mice but occurred normally in Tcra(-/-) mice. Imiquimod-induced skin pathology was also significantly decreased in Tcrd(-/-) mice. Perhaps further promoting disease progression, IL-23 stimulated dermal gammadelta T cell expansion. In psoriasis patients, gammadelta T cells were greatly increased in affected skin and produced large amounts of IL-17. Thus, IL-23-responsive dermal gammadelta T cells are the major IL-17 producers in the skin and may represent a novel target for the treatment of psoriasis. |
