01909nas a2200289   4500000000100000008004100001260001200042653001100054653001000065653000800075653001100083653002200094653001200116100001000128700001000138700000900148700000900157700000900166700001000175700001100185245012400196856008100320300001100401490000700412520118600419022001401605       2022                            d  c01/202210aIL-17A10aIL-2310aROR10aDermis10agamm delta T cell10aleprosy1 aLiu Y1 aShi C1 aMa S1 aMa Y1 aLu X1 aZhu J1 aYang D00aThe protective role of tissue-resident interleukin 17A-producing gamma delta T cells in Mycobacterium leprae infection.  uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9644052/pdf/fimmu-13-961405.pdf  a9614050 v133 a<p>Mycobacterium is a kind of disease-causing bacteria and results in leprosy in human. Gamma delta (γδ) T cell is a T-cell subset that is presented in both human dermis and epidermis. These cells bridge innate and adaptive immune responses and play critical roles in regulating anti-microbial defense, wound healing, and skin inflammation. Here, we investigated skin resident γδ T cells in patients with leprosy. Our data showed that γδ T cells significantly accumulated in skin lesions of leprosy patients with tuberculoid (TT) form. IL-23 can predominantly stimulate dermal γδ T cells to produce interleukin 17 (IL-17), a cytokine which may lead to disease protection. These γδ T cells expressed a specific set of surface molecules, and majority of these cells were Vδ1. Also, IL-23 can stimulate the expansion of dermal γδ T cells expansion. Moreover, our results revealed that the transcription factor RORγt was responsible for IL-17A expression in leprosy lesion. Therefore, these data indicated that IL-23-responsive dermal γδ T cells were the major resource of IL-17A production in the skin and could be a potential target in the treatment of leprosy.</p>
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