Obesity Drives Th17 Cell Differentiation by Inducing the Lipid Metabolic Kinase, ACC1

• DOI: 10.1016/j.celrep.2015.07.014
• Publication Date: 2015-07-30T19:57:58Z
• Authors: Yusuke Endo; Hikari K. Asou; Nao Matsugae; Kiyoshi Hirahara; Kenta Shinoda; Damon J. Tumes; Hirotake Tokuyama; Koutaro Yokote; Toshinori Nakayama
• Keywords: CD4-Positive T-Lymphocytes; 0301 basic medicine; 2. Zero hunger; obesity; QH301-705.5; Cell Differentiation; 3. Good health; cell differentiation; Mice; 03 medical and health sciences; Acetyltransferases; Animals; Leukocyte Common Antigens; Th17 Cells; Obesity; Th17 cells; Biology (General); Cells, Cultured

Chronic inflammation due to obesity contributes the development of metabolic diseases, autoimmune and cancer. Reciprocal interactions between systems immune cells have pivotal roles in pathogenesis obesity-associated although mechanisms regulating inflammatory diseases are still unclear. In present study, we performed transcriptional profiling memory phenotype CD4 T high-fat-fed mice identified acetyl-CoA carboxylase 1 (ACC1, gene product Acaca) as an essential regulator Th17 cell differentiation vitro pathogenicity vivo. ACC1 modulates DNA binding RORγt target genes differentiating cells. addition, found a strong correlation IL-17A-producing CD45RO+CD4 expression ACACA obese subjects. Thus, confers appropriate function through fatty acid synthesis regulates obesity-related pathology