Abstract
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 Vγ4+γδ-T cells. Adiponectin directly acts on murine dermal γδ-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.
Highlights
Accumulating epidemiologic evidence has revealed that metabolic syndrome is an independent risk factor for psoriasis development and is associated with more severe psoriasis
Serum adiponectin levels are decreased in psoriasis patients compared with healthy controls and its levels increase along with the improvement of dermatitis after successful treatments, including anti-tumour necrosis factor (TNF)-a agents, suggesting that adiponectin negatively regulates psoriasis progression[30,31]
Immunohistochemistry analyses revealed that infiltrating cells in the upper dermis were CD3 or major histocompatibility complex class II positive, and that cell counts for these positive cells were significantly increased in adiponectin-deficient mice compared with wild-type mice (Fig. 1d)
Summary
Accumulating epidemiologic evidence has revealed that metabolic syndrome is an independent risk factor for psoriasis development and is associated with more severe psoriasis. Immune cells and cytokines, when released into the systemic circulation, may alter the function of endothelial and haematopoietic cells, leading to the increase in the risk of insulin resistance and atherosclerosis This inflammatory cascade is named ‘psoriatic march’, and psoriasis patients are considered to be at higher risk of developing metabolic syndrome[11]. Considered as an organ for energy storage in the past, is accepted as an active endocrine and immune organ, which produces various bioactive molecules, named adipokines[18,19] These adipokines, in cooperation with macrophages and T cells, cause adipose tissue inflammation and develop metabolic syndrome. Adiponectin directly acts on dermal gd-T cells to suppress IL-17 production These results are in agreement with human data displaying the decreased level of adiponectin in subcutaneous fat and skin tissue of psoriasis patients. Numerous reports have reported anti-inflammatory aspects of adiponectin on a variety of cell types, our data provides new evidence that adiponectin has an anti-inflammatory effect on T cells and regulates skin inflammation
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
