01731nas a2200229   4500000000100000008004100001260001200042653001000054653001200064653001500076100001000091700000900101700001000110700001000120700000900130700000900139700001000148700001100158245008600169520123200255022001401487       2022                            d  c06/202210aIL-2310aleprosy10aTh17 Cells1 aShi C1 aMa S1 aBai J1 aLiu Y1 aMa Y1 aLu X1 aZhu J1 aYang D00aElevated IL-23 in skin promotes IL-23 derived Th17 responses in leprosy patients.3 a<p>Leprosy is an infectious disease caused by non-cultivable bacteria Mycobacterium leprae. Th17 cells play vital roles during pathogenesis of leprosy reactions and IL-23 is involved in Th17 cell differentiation. Although previous studies have reported the participation of IL-23 in leprosy patients in peripheral blood, the role of this cytokine in skin has not yet been described for the disease. In this study, we first evaluated IL-23 expression in the skin of patients with leprosy. Data showed that in keratinocytes, endothelial cells, and macrophages, IL-23 expression was markedly higher in patients compared to that in the normal skin controls. Also, leprosy patients presented higher percentage of IL-17A-producing IL-23R + CD4 T cells than healthy donors. IL-23R blocking induced markedly downregulated IL-17A secretion in leprosy patients but not in healthy donors. Furthermore, TGF- β expression was significantly elevated after IL-23R blocking. Overall, this study establishes that Th17 cells produce IL-17A in an IL-23 dependent manner in the skin of leprosy patients and provides more focused treatment strategies for Mycobacterium leprae. This article is protected by copyright. All rights reserved.</p>
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