Zinc deficiency drives Th17 polarization and promotes loss of Treg cell function |
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| Institution: | 1. Department of Pharmacology, School of Pharmacy, Nantong University, #19 Qixiu Road, Nantong, Jiangsu Province, China 226001;2. Department of Cardiology, Suzhou Kowloon Hospital of Shanghai Jiaotong University School of Medicine, #118 Wansheng Street, Suzhou 215021, Jiangsu, China;3. Invasive Technology Department, Nantong First People''s Hospital, The Second Affiliated Hospital of Nantong University, #6 North Road Hai''er Xiang, Nantong, Jiangsu Province, China 226001;1. Department of Experimental Diabetology, German Institute of Human Nutrition Potsdam-Rehbrücke (DIfE), Arthur-Scheunert-Allee 114-116, 14558 Nuthetal, Germany;2. German Center for Diabetes Research (DZD), Ingolstädter Landstraße 1, 85764 Neuherberg, Germany;3. Institute of Nutritional Science, University of Potsdam, Arthur-Scheunert-Allee 114-116, 14558 Nuthetal, Germany;1. Department of Medicine, University of California, Irvine, CA 92697;2. Department of Physiology/Biophysics, University of California, Irvine, CA 92697;3. VA Medical Center, Long Beach, CA 90822;4. Department of Cell Biology, Neurobiology & Anatomy, Medical College of Wisconsin, WI 53226;1. Human Nutrition Program, Department of Human Sciences, The Ohio State University, Columbus, OH 43210, USA;2. Biofortis, Merieux NutriSciences, Addison, IL 60101, USA;3. Department of Biological Chemistry and Pharmacology, The Ohio State University, Columbus, OH 43210, USA;1. Laboratory of Biochemistry and Human nutrition, Agrocampus-Ouest, 35042, Rennes, France;2. French Dairy Interbranch Organization (CNIEL), Technical and Scientific Department, 75314, Paris, France;1. Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, N1G2W1, Canada;2. Division of Nutritional Sciences, University of Illinois, Urbana, IL, USA |
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| Abstract: | A high number of illnesses and disorders are connected to zinc deficiency. Equally, T cell polarization and a balance between different T helper (Th) cell subsets are essential. Therefore, in this study, the influence of zinc deficiency on T cell polarization and on respective signaling pathways was investigated. We uncovered a significantly increased number of regulatory T cells (Treg) and Th17 cells in expanded T cells during zinc deficiency after 3 days of combined treatment with IL-2 and TGF-β1 (Treg) or IL-6 and TGF-β1 (Th17). No difference in Th1 and Th2 cell polarization between zinc-deficient and zinc-adequate status was prominent. On the molecular level, Smad signaling was significantly enhanced by stimulation with TGF-β1/IL-6 during zinc deficiency compared to adequate zinc condition. This represents an explanation for the elevated Th17 cell numbers associated with autoimmune disease especially during zinc deficiency. Moreover, Treg cell numbers are increased during zinc deficiency as well. However, those cells might be nonfunctional since a lower expression of miR-146a was uncovered compared to normal zinc concentrations. In summary, an adequate zinc homeostasis is fundamental to slow down or probably stop the progression of autoimmune diseases and infections. Therefore, supplementing zinc might be a therapeutic approach to dampen autoimmune diseases connected to Th17 cells. |
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