| First Author | Shibata S | Year | 2015 |
| Journal | Nat Commun | Volume | 6 |
| Pages | 7687 | PubMed ID | 26173479 |
| Mgi Jnum | J:224460 | Mgi Id | MGI:5662318 |
| Doi | 10.1038/ncomms8687 | Citation | Shibata S, et al. (2015) Adiponectin regulates psoriasiform skin inflammation by suppressing IL-17 production from gammadelta-T cells. Nat Commun 6:7687 |
| abstractText | Accumulating epidemiologic evidence has revealed that metabolic syndrome is an independent risk factor for psoriasis development and is associated with more severe psoriasis. Adiponectin, primarily recognized as a metabolic mediator of insulin sensitivity, has been newly drawing attention as a mediator of immune responses. Here we demonstrate that adiponectin regulates skin inflammation, especially IL-17-related psoriasiform dermatitis. Mice with adiponectin deficiency show severe psoriasiform skin inflammation with enhanced infiltration of IL-17-producing dermal Vgamma4+gammadelta-T cells. Adiponectin directly acts on murine dermal gammadelta-T cells to suppress IL-17 synthesis via AdipoR1. We furthermore demonstrate here that the adiponectin level of skin tissue as well as subcutaneous fat is decreased in psoriasis patients. IL-17 production from human CD4- or CD8-positive T cells is also suppressed by adiponectin. Our data provide a regulatory role of adiponectin in skin inflammation, which would imply a mechanism underlying the relationship between psoriasis and metabolic disorders. |
