| First Author | Mabuchi T | Year | 2011 |
| Journal | J Immunol | Volume | 187 |
| Issue | 10 | Pages | 5026-31 |
| PubMed ID | 21984702 | Mgi Jnum | J:179642 |
| Mgi Id | MGI:5302790 | Doi | 10.4049/jimmunol.1101817 |
| Citation | Mabuchi T, et al. (2011) Epidermal CCR6+ gammadelta T cells are major producers of IL-22 and IL-17 in a murine model of psoriasiform dermatitis. J Immunol 187(10):5026-31 |
| abstractText | Cytokine components of Th17 pathway play vital roles in human psoriasis. Although much is known about TCR alphabeta T cells in psoriasis, the role of unconventional T cells, including gammadelta T cells, is unclear. In this study, using an IL-23 skin injection model of psoriasiform dermatitis in mice, we demonstrate that IL-22, IL-17A, and the IL-23R were highly enriched in a population of CCR6(+), TCR gammadelta-low expressing (GDL) T cells that accumulated in the epidermis after IL-23 injections. GDL cells were distinct from resident TCR gammadelta-high, Vgamma3(+),CCR6(-) T cells in the epidermis that did not change appreciably in numbers following IL-23 injection. Large numbers of CCR6(+) cells were detected at or above the level of the epidermal basement membrane by confocal microscopy 5 d after repeated IL-23 injections at the same time GDL cells increased in numbers in the epidermis. TCR delta-deficient mice (lacking gammadelta T cells) exhibited decreased ear swelling and downregulated expression of IL-22 and IL-17A in the epidermis following IL-23 injection. Our data suggest that a subset of gammadelta T cells play a critical role in IL-23-mediated psoriasiform dermatitis. |
