Type II NKT cells stimulate diet-induced obesity by mediating adipose tissue inflammation, steatohepatitis and insulin resistance.
Type II NKT cells stimulate diet-induced obesity by mediating adipose tissue inflammation, steatohepatitis and insulin resistance.
复制标题
II型NKT细胞通过介导脂肪组织炎症，脂肪性肝炎和胰岛素抵抗来刺激饮食诱导的肥胖。
DOI：
10.1371/journal.pone.0030568
复制
发表时间：
2012
期刊：
影响因子：
3.7
通讯作者：
Iwabuchi K
中科院分区：
文献类型：
--
作者：
Satoh M;Andoh Y;Clingan CS;Ogura H;Fujii S;Eshima K;Nakayama T;Taniguchi M;Hirata N;Ishimori N;Tsutsui H;Onoé K;Iwabuchi K
肥胖症的进展伴随着涉及先天性和获得性免疫的慢性炎症过程。自然杀伤T（NKT）细胞识别脂质抗原，也分布在脂肪组织中。为了研究NKT细胞在肥胖发生中的作用，C57 BL/6小鼠（野生型; WT）和两种NKT细胞缺陷型小鼠，即缺乏I型亚群的Jα18−/−小鼠和缺乏I型和II型亚群的CD 1d −/−小鼠，被喂食高脂饮食（HFD）。与喂食HFD的WT或Jα18−/−小鼠相比，CD 1d −/−小鼠的体重增加最少，性腺周围和棕色脂肪组织以及肝脏的重量最少。在组织学上，CD 1d −/−小鼠的脂肪细胞明显小于WT或Jα18−/−小鼠，肝脂肪变性明显较轻。当WT小鼠喂食HFD时，脂肪组织中的NK1.1+TCRβ+细胞数量增加，并且大多数是不变的Vα 14 J α18阴性。CD 11b+巨噬细胞（Mφ）是脂肪组织浸润中的另一个主要细胞亚群，分为F4/80 high和F4/80 low细胞。脂肪组织中的F4/80 low-M φ亚群在CD 1d −/−小鼠中增加，并且该群体可能发挥抗炎作用。CD 1d −/−小鼠的葡萄糖耐受不良和胰岛素抵抗并没有像喂食HFD的WT或Jα18−/−小鼠那样加重，这可能是由于炎症和肥胖程度较低。总的来说，我们的研究结果提供了证据表明，II型NKT细胞启动肝脏和脂肪组织的炎症，并加剧肥胖的过程，导致胰岛素抵抗。
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 F4/80high and F4/80low cells. The F4/80low-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.
登录
查看更多内容
影响因子：
3.7
作者：
Armougom F;Henry M;Vialettes B;Raccah D;Raoult D
通讯作者：
Raoult D
影响因子：
32.4
作者：
Mendiratta, SK;Martin, WD;VanKaer, L
通讯作者：
VanKaer, L
影响因子：
4.3
作者：
Bassaganya-Riera, Josep;Misyak, Sarah;Hontecillas, Raquel
通讯作者：
Hontecillas, Raquel
影响因子：
7.3
作者：
Elinav, E;Pappo, O;Ilan, Y
通讯作者：
Ilan, Y
通过靶向独特的无引起的CD1D反应T细胞群体对硫化物的反应性，预防自身免疫性。
影响因子：
15.3
作者：
Jahng, A;Maricic, I;Aguilera, C;Cardell, S;Halder, RC;Kumar, V
通讯作者：
Kumar, V