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Obesity Drives Th17 Cell Differentiation by Inducing the Lipid Metabolic Kinase, ACC1
Open accessAbstract
Chronic inflammation due to obesity contributes to the development of metabolic diseases, autoimmune diseases, and cancer. Reciprocal interactions between metabolic systems and immune cells have pivotal roles in the pathogenesis of obesity-associated diseases, although the mechanisms regulating obesity-associated inflammatory diseases are still unclear. In the present study, we performed transcriptional profiling of memory phenotype CD4 T cells in high-fat-fed mice and identified acetyl-CoA carboxylase 1 (ACC1, the gene product of Acaca) as an essential regulator of Th17 cell differentiation in vitro and of the pathogenicity of Th17 cells in vivo. ACC1 modulates the DNA binding of RORγt to target genes in differentiating Th17 cells. In addition, we found a strong correlation between IL-17A-producing CD45RO(+)CD4 T cells and the expression of ACACA in obese subjects. Thus, ACC1 confers the appropriate function of RORγt through fatty acid synthesis and regulates the obesity-related pathology of Th17 cells.
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Methionine Metabolism Shapes T Helper Cell Responses through Regulation of Epigenetic Reprogramming
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The Intestine Harbors Functionally Distinct Homeostatic Tissue-Resident and Inflammatory Th17 Cells
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Immunity, Hypoxia, and Metabolism–the Ménage à Trois of Cancer: Implications for Immunotherapy
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Metadata
- Authors
- Endo, Y., Asou, H. K., Matsugae, N., Hirahara, K., Shinoda, K., Tumes, D. J., Tokuyama, H., Yokote, K., & Nakayama, T.
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2015-08
- Volume
- 12
- Issue
- 6
- Pages
- 1042-1055
- ISSN
- 2211-1247 (ISSN-L)
- OpenAlex
- W1950312625
- Cited by
- 249
- References
- 16
- FWCI
- 6.18
- Type
- journal article
- Language
- en
- Open access
- gold
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- Endo, Y., Asou, H. K., Matsugae, N., Hirahara, K., Shinoda, K., Tumes, D. J., Tokuyama, H., Yokote, K., & Nakayama, T. (2015). Obesity Drives Th17 Cell Differentiation by Inducing the Lipid Metabolic Kinase, ACC1. Cell Reports. https://doi.org/10.1016/j.celrep.2015.07.014
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