Psoriasis is a common, chronic inflammatory skin disease characterized by epidermal hyperplasia via the IL-23/IL-17 axis. Various studies have indicated the association between obesity and psoriasis, however, the underlying mechanisms remains unclarified. To this end, we focused on high-fat diet (HFD) in this study, because HFD is suggested as a contributor to obesity, and HFD-fed mice exhibit exacerbated psoriatic dermatitis. Using murine imiquimod (IMQ)-induced psoriasis and HFD-induced obesity models, we have revealed a novel mechanism of HFD-induced exacerbation of psoriatic dermatitis. HFD-fed mice exhibited aggravated psoriatic dermatitis, which was accompanied with increased accumulation of IL-17A-producing Vγ4+ γδ T cells in the skin. HFD also induced the increase of Vγ4+ γδ T cells in other organs such as skin draining lymph nodes, which preceded the increase of them in the skin. In addition, HFD-fed mice displayed increased expression of several γδ T cell-recruiting chemokines in the skin. On the other hand, ob/ob mice, another model of murine obesity on normal diet, did not exhibit aggravated psoriatic dermatitis nor accumulation of γδ T cells in the dermis. These results indicate that HFD is a key element in exacerbation of IMQ-induced psoriatic dermatitis, and further raise the possibility of HFD as a factor that links obesity and psoriasis.

Disclosure of potential conflict of interest: F. de Blay reports grants from Stallergenes-Greer and Chiesi and personal fees from ALK, Mundipharma, and Novartis, during the conduct of the study; and is a board member for Stallergenes-Greer, Novartis, ALK, Mundipharma, Medapharma, Boehringer, and Teva. M. Jutel reports lecture fees from ALK-Abello; lecture fees, advisory board, and clinical investigator fees from Allergopharma; lecture fees and clinical investigator fees from Stallergenes; advisory board and clinical investigator fees from Anergis; advisory board fees from Biomay and UCB; and clinical investigator fees from HAL, Astra-Zeneka, GSK, Novartis, Teva, Vectura, Tekada, Roche, Janssen, Medimmune, Allergy Therapeutics, Circassia, Leti, and Chiesi. L. Jacobsen and M. Worm received money for consulting fees and study preparation from Anergis SA. L. Jacobsen received money for study preparation from Anergis SA. M. Worm was paid for consultancy outside of this research by Anergis SA. A. Kettner, G. DellaCorte, V. Charlon, C. Reymond, and K. Simonsen are employees of Anergis SA and have stock options with this company. V. Charlon received travel/accommodations/meeting expenses from Anergis SA unrelated to this research. F. Spertini has stock/stock options with Anergis SA; received support for travel to meetings for the study or other purposes from Anergis SA; has patents (planned, pending, or issued) and received royalties from CHUV, Lausanne, CH; and is a funder of the company Anergis SA, which supported this study.

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We describe a case of H syndrome with massive skin involvement, retroperitoneal fibrosis and Raynaud's phenomenon. A 48-year-old man with parents of a consanguineous marriage, first appeared with decreased urine output, skin sclerosis on his inner thighs and short stature (142 cm, 47 kg). The patient had suffered from hearing loss since the age of 1 year, and his secondary sexual characteristics had not developed. Computed tomography showed periaortic fibrosis, bilateral ureteral stenosis, hydronephrosis and sclerosis of the germinal cords. A biopsy from the retroperitoneal mass revealed remarkable fibrosis with chronic inflammatory cells. Biopsies from the skin lesion showed thick collagen bundles through the dermis and lymphohistiocytic infiltration with numerous plasma cells. Serum inflammatory markers, such as C-reactive protein, vascular endothelial factor, transforming growth factor-β and soluble interleukin-2 receptor, were elevated. Prednisolone was effective in treating skin lesions and in lowering serum inflammatory markers. After a long period of follow up, genomic DNA of the patient was obtained, and we identified a homozygous mutation in exon 5, c.625G>A, which caused transition of glycine to arginine, p.Gly208Arg, in the patient, but not in DNA samples from another 50 healthy individuals. This is the first case of H syndrome with Raynaud's phenomenon and retroperitoneal fibrosis, and the first Japanese case of H syndrome reported in the English published work with a novel mutation in the SLC29A3 gene.