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Obesity drives Th17 cell differentiation by inducing the lipid metabolic kinase, ACC1

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dc.contributor.authorEndo, Y.
dc.contributor.authorAsou, H.K.
dc.contributor.authorMatsugae, N.
dc.contributor.authorHirahara, K.
dc.contributor.authorShinoda, K.
dc.contributor.authorTumes, D.J.
dc.contributor.authorTokuyama, H.
dc.contributor.authorYokote, K.
dc.contributor.authorNakayama, T.
dc.date.issued2015
dc.description.abstractChronic 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 RORgt to target genes in differentiating Th17 cells. In addition, we found a strong correlation between IL-17Aproducing CD45RO+CD4 T cells and the expression of ACACA in obese subjects. Thus, ACC1 confers the appropriate function of RORgt through fatty acid synthesis and regulates the obesity-related pathology of Th17 cells.
dc.identifier.citationCell reports, 2015; 12(6):1042-1055
dc.identifier.doi10.1016/j.celrep.2015.07.014
dc.identifier.issn2211-1247
dc.identifier.issn2211-1247
dc.identifier.orcidTumes, D.J. [0000-0001-5709-857X]
dc.identifier.urihttps://hdl.handle.net/11541.2/132028
dc.language.isoen
dc.publisherCell Press
dc.relation.fundingGlobal Center for Education and Research in Immune System Regulation and Treatment
dc.relation.fundingJapan Science and Technology Agency (JST)
dc.relation.fundingCREST
dc.relation.fundingMinistry of Education, Culture, Sports, Science and Technology (MEXT Japan) 26221305
dc.relation.fundingMinistry of Education, Culture, Sports, Science and Technology (MEXT Japan) 21390147
dc.relation.fundingMinistry of Education, Culture, Sports, Science and Technology (MEXT Japan) 26293165
dc.relation.fundingMinistry of Education, Culture, Sports, Science and Technology (MEXT Japan) 24592083
dc.relation.fundingMinistry of Education, Culture, Sports, Science and Technology (MEXT Japan) 24790461
dc.relation.fundingMinistry of Education, Culture, Sports, Science and Technology (MEXT Japan) 25860352
dc.relation.fundingMinistry of Education, Culture, Sports, Science and Technology (MEXT Japan) 23890030
dc.relation.fundingMinistry of Education, Culture, Sports, Science and Technology (MEXT Japan) 25893032
dc.relation.fundingMinistry of Education, Culture, Sports, Science and Technology (MEXT Japan) 26670362
dc.relation.fundingMinistry of Education, Culture, Sports, Science and Technology (MEXT Japan) 26115009
dc.relation.fundingMinistry of Health, Labor and Welfare
dc.relation.fundingThe Astellas Foundation for Research on Metabolic Disorders
dc.rightsCopyright 2015 The Authors. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/)
dc.source.urihttps://doi.org/10.1016/j.celrep.2015.07.014
dc.subjectobesity
dc.subjectTh17 cells
dc.subjectcell differentiation
dc.subjectCD4-Positive T-Lymphocytes
dc.subjectCells, Cultured
dc.subjectAnimals
dc.subjectMice
dc.subjectAcetyltransferases
dc.subjectLeukocyte Common Antigens
dc.titleObesity drives Th17 cell differentiation by inducing the lipid metabolic kinase, ACC1
dc.typeJournal article
pubs.publication-statusPublished
ror.mmsid9916195311901831

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