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10.1016/j.jid.2016.02.816

http://scihub22266oqcxt.onion/10.1016/j.jid.2016.02.816
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C4992618!4992618!27236103
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suck abstract from ncbi


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pmid27236103      J+Invest+Dermatol 2016 ; 136 (9): 1801-10
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  • Myeloid-derived Suppressor Cells in Psoriasis Are an Expanded Population Exhibiting Diverse T cell-Suppressor Mechanisms #MMPMID27236103
  • Cao LY; Chung JS; Teshima T; Feigenbaum L; Cruz PD; Jacobe HT; Chong BF; Ariizumi K
  • J Invest Dermatol 2016[Sep]; 136 (9): 1801-10 PMID27236103show ga
  • Psoriasis vulgaris is an inflammatory skin disease caused by hyper-activated T-cells regulated by positive and negative mechanisms; while the former has been much studied, but the latter has not. We studied the regulatory mechanism mediated by myeloid-derived suppressor cells (MDSCs), especially having shown that MDSCs expanded in melanoma patients express DC-HIL, a critical mediator of T-cell suppressor function. We examined expansion of DC-HIL+ MDSCs in psoriasis and characterized their functional properties. Frequency of DC-HIL+ monocytic MDSCs (CD14+HLA-DRno/low) in blood and skin was markedly increased in psoriatic patients vs. healthy controls, but there was no statistically significant relationship with disease severity (PASI score). Blood DC-HIL+ MDSC levels in the untreated patients were significantly higher than the treated patients. Compared to melanoma-derived MDSCs, psoriatic MDSCs exhibited significantly reduced suppressor function, and were less dependent on DC-HIL, but capable of inhibiting proliferation and IFN-? and IL-17 responses of autologous T-cells. Psoriatic MDSCs were functionally diverse among patients in their ability to suppress allogeneic T-cells and use of either IL-17/arginase I or IFN-?/iNOS axis as suppressor mechanisms. Thus DC-HIL+ MDSCs are expanded in psoriasis patients, and their mechanistic heterogeneity and relative functional deficiency may contribute to the development of psoriasis.
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