827 Psoriasis exacerbation by obesity reflects reduced adiponectin regulation of PPAR-γ/Th17 pathway activation and is reversal by adiponectin receptor agonism

Abstract

Although obesity-related deficiency of adipokines is known to contribute to increased psoriasis severity and decreased clinical response to interventions, the mechanism by which it exacerbates psoriasis is poorly defined. We hypothesized that adipokines suppress the activation of innate immune responses in keratinocytes and skin-resident Th17/γδ T cells. In preliminary studies, we confirmed that diet-induced obese (DIO) mice had significantly lower serum adiponectin levels than lean mice when subjected to topical imiquimod (IMQ) treatments to induce the psoriasis-like disease, supporting the use of this model for studies.