These authors contributed equally to this work.
Obesity predisposes to Th17 bias
Version of Record online: 6 AUG 2009
Copyright © 2009 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
European Journal of Immunology
Volume 39, Issue 9, pages 2629–2635, September 2009
How to Cite
Winer, S., Paltser, G., Chan, Y., Tsui, H., Engleman, E., Winer, D. and Dosch, H.-M. (2009), Obesity predisposes to Th17 bias. Eur. J. Immunol., 39: 2629–2635. doi: 10.1002/eji.200838893
- Issue online: 27 AUG 2009
- Version of Record online: 6 AUG 2009
- Manuscript Accepted: 24 JUN 2009
- Manuscript Revised: 12 JUN 2009
- Manuscript Received: 6 SEP 2008
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.