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Type II NKT Cells Stimulate Diet-Induced Obesity by Mediating Adipose Tissue Inflammation, Steatohepatitis and Insulin Resistance

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Title: Type II NKT Cells Stimulate Diet-Induced Obesity by Mediating Adipose Tissue Inflammation, Steatohepatitis and Insulin Resistance
Authors: Satoh, Masashi Browse this author
Andoh, Yasuhiro Browse this author
Clingan, Christopher Stuart Browse this author
Ogura, Hisako Browse this author
Fujii, Satoshi Browse this author
Eshima, Koji Browse this author
Nakayama, Toshinori Browse this author
Taniguchi, Masaru Browse this author
Hirata, Noriyuki Browse this author
Ishimori, Naoki Browse this author →KAKEN DB
Tsutsui, Hiroyuki Browse this author →KAKEN DB
Onoé, Kazunori Browse this author →KAKEN DB
Iwabuchi, Kazuya Browse this author →KAKEN DB
Issue Date: 22-Feb-2012
Publisher: Public Library of Science
Journal Title: PLoS One
Volume: 7
Issue: 2
Start Page: e30568
Publisher DOI: 10.1371/journal.pone.0030568
Abstract: The progression of obesity is accompanied by a chronic inflammatory process that involves both innate and acquired immunity. Natural killer T (NKT) cells recognize lipid antigens and are also distributed in adipose tissue. To examine the involvement of NKT cells in the development of obesity, C57BL/6 mice (wild type; WT), and two NKT-cell-deficient strains, Jα18^[-/-] mice that lack the type I subset and CD1d^[-/-] mice that lack both the type I and II subsets, were fed a high fat diet (HFD). CD1d^[-/-] mice gained the least body weight with the least weight in perigonadal and brown adipose tissue as well as in the liver, compared to WT or Jα18^[-/-] mice fed an HFD. Histologically, CD1d^[-/-] mice had significantly smaller adipocytes and developed significantly milder hepatosteatosis than WT or Jα18^[-/-] mice. The number of NK1.1^[+]TCRβ^[+] cells in adipose tissue increased when WT mice were fed an HFD and were mostly invariant Vα14Jα18-negative. CD11b^[+] macrophages (Mφ) were another major subset of cells in adipose tissue infiltrates, and they were divided into F4/80^[high] and F4/80^[low] cells. The F4/80^[low]-Mφ subset in adipose tissue was increased in CD1d^[-/-] mice, and this population likely played an anti-inflammatory role. Glucose intolerance and insulin resistance in CD1d^[-/-] mice were not aggravated as in WT or Jα18^[-/-] mice fed an HFD, likely due to a lower grade of inflammation and adiposity. Collectively, our findings provide evidence that type II NKT cells initiate inflammation in the liver and adipose tissue and exacerbate the course of obesity that leads to insulin resistance.
Rights: http://creativecommons.org/licenses/by/3.0/
Type: article
URI: http://hdl.handle.net/2115/49209
Appears in Collections:遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 岩渕 和也

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