Cutting edge: IL-25 elicits innate lymphoid type 2 and type II NKT cells that regulate obesity in mice.

Cutting edge: IL-25 elicits innate lymphoid type 2 and type II NKT cells that regulate obesity in mice.
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DOI:
10.4049/jimmunol.1301176
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发表时间:
2013-12-01
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
通讯作者:
Fallon PG
Fallon PG
中科院分区:
其他
文献类型:
--
作者:
Hams E;Locksley RM;McKenzie AN;Fallon PG

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内脏脂肪组织(VAT)的细胞组成和VAT内这些细胞释放的细胞因子在调节肥胖和代谢动态平衡方面具有重要意义。我们展示了IL-25反应的先天细胞的重要性,它释放Th2细胞因子IL-13,在饮食诱导肥胖的小鼠模型中调节体重和血糖稳态。使用IL-25治疗肥胖小鼠可导致体重减轻和糖耐量提高,并与ILC2、I型和II型自然杀伤T细胞(NKT)、嗜酸性粒细胞和激活的巨噬细胞(AAM)在VAT中的渗透增加有关。通过消耗肥胖RAG1−/−小鼠的ILC2,我们观察到体重增加和糖耐量减低加剧。相反,将ILC2或I型或II型NKT细胞转移到肥胖小鼠体内可诱导一过性体重减轻并稳定血糖稳态。我们的数据确定了一种机制,即IL-25激发产生IL-13的固有细胞调节脂肪组织中的炎症,并防止饮食诱导的肥胖。
The cellular composition of visceral adipose tissue (VAT) and release of cytokines by such cells within VAT has been implicated in regulating obesity and metabolic homeostasis. We show the importance of IL-25-responsive innate cells, that release the Th2 cytokine IL-13, in regulating weight and glucose homeostasis in mouse models of diet-induced obesity. Treating obese mice with IL-25 induces weight loss and improves glucose tolerance, and is associated with increased infiltration of ILC2s, type I and type II natural killer T (NKT) cells, eosinophils and alternatively activated macrophages (AAM) into the VAT. By depleting ILC2 in obese Rag1−/− mice we observe exacerbated weight gain and glucose intolerance. Conversely, transferring ILC2 or type I or type II NKT cells into obese mice induces transient weight loss and stabilizes glucose homeostasis. Our data identifies a mechanism whereby IL-25 eliciting IL-13 producing innate cells regulates inflammation in adipose tissue and prevents diet-induced obesity.
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