| First Author | Mabuchi T | Year | 2013 |
| Journal | J Invest Dermatol | Volume | 133 |
| Issue | 1 | Pages | 164-71 |
| PubMed ID | 22895364 | Mgi Jnum | J:196524 |
| Mgi Id | MGI:5488686 | Doi | 10.1038/jid.2012.260 |
| Citation | Mabuchi T, et al. (2013) CCR6 is required for epidermal trafficking of gammadelta-T cells in an IL-23-induced model of psoriasiform dermatitis. J Invest Dermatol 133(1):164-71 |
| abstractText | A subset of CC chemokine receptor-6(+) (CCR6(+)), gammadelta-low (GDL) T cells that express Th17 cytokines in mouse skin participates in IL-23-induced psoriasiform dermatitis. We use CCR6-deficient (knockout, KO) and wild-type (WT) mice to analyze skin trafficking patterns of GDL T cells and function-blocking mAbs to determine the role of CCR6 in IL-23-mediated dermatitis. Herein, CCL20 was highly upregulated in IL-23-injected WT mouse ear skin as early as 24 hours after initial treatment, and large numbers of CCR6(+) cells were observed in the epidermis of IL-23-injected WT mice. Anti-CCL20 mAbs reduced psoriasiform dermatitis and blocked recruitment of GDL T cells to the epidermis. In CCR6 KO mice, GDL T cells failed to accumulate in the epidermis after IL-23 treatment, but the total numbers of GDL T cells in the dermis of WT and CCR6 KO mice were equivalent. There was an approximately 70% reduction in the proportion of IL-22(+) GDL T cells in the dermis of CCR6 KO mice (vs WT mice), suggesting that effector function and epidermal recruitment of GDL T cells are impaired in CCR6-deficient mice. Thus, these data show that CCR6 regulates epidermal trafficking of gammadelta-T-cell subsets in the skin and suggest the potential of CCR6 as a therapeutic target for psoriasis. |
