Obesity predisposes to Th17 bias |
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Authors: | Shawn Winer Geoff Paltser Yin Chan Hubert Tsui Edgar Engleman Daniel Winer H‐Michael Dosch |
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Institution: | 1. Neuroscience and Mental Health program, Research Institute, The Hospital for Sick Children, University of Toronto Departments of Pediatrics & Immunology, Toronto, Ontario Canada;2. Department of Pathology, Stanford University School of Medicine, Palo Alto, CA, USA |
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Abstract: | Obesity is associated with numerous inflammatory conditions including atherosclerosis, autoimmune disease and cancer. Although the precise mechanisms are unknown, obesity‐associated rises in TNF‐α, IL‐6 and TGF‐β are believed to contribute. Here we demonstrate that obesity selectively promotes an expansion of the Th17 T‐cell sublineage, a subset with prominent pro‐inflammatory roles. T‐cells from diet‐induced obese mice expand Th17 cell pools and produce progressively more IL‐17 than lean littermates in an IL‐6‐dependent process. The increased Th17 bias was associated with more pronounced autoimmune disease as confirmed in two disease models, EAE and trinitrobenzene sulfonic acid colitis. In both, diet‐induced obese mice developed more severe early disease and histopathology with increased IL‐17+ T‐cell pools in target tissues. The well‐described association of obesity with inflammatory and autoimmune disease is mechanistically linked to a Th17 bias. |
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Keywords: | Autoimmunity IL‐17 Obesity |
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