Innate lymphoid type 2 cells sustain visceral adipose tissue eosinophils and alternatively activated macrophages.
Innate lymphoid type 2 cells sustain visceral adipose tissue eosinophils and alternatively activated macrophages.
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DOI：
10.1084/jem.20121964
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发表时间：
2013-03-11
期刊：
影响因子：
--
通讯作者：
Locksley RM
中科院分区：
文献类型：
--
作者：
Molofsky AB;Nussbaum JC;Liang HE;Van Dyken SJ;Cheng LE;Mohapatra A;Chawla A;Locksley RM
先天性淋巴2型细胞通过产生IL-5和IL-13维持内脏脂肪中的嗜酸性粒细胞和交替活化的巨噬细胞。内脏脂肪组织（VAT）中的嗜酸性粒细胞与代谢稳态和交替激活的巨噬细胞（AAM）的维持有关。嗜酸性粒细胞的缺乏可导致实验动物肥胖和全身胰岛素抵抗，但什么维持脂肪组织中的嗜酸性粒细胞尚不清楚。我们发现，白细胞介素-5（IL-5）缺乏深刻损害增值税嗜酸性粒细胞的积累，并导致增加肥胖和胰岛素抵抗时，动物被放置在一个高脂肪饮食。先天性淋巴样2型细胞（ILC 2）驻留在VAT中，是IL-5和IL-13的主要来源，其促进嗜酸性粒细胞和AAM的积累。ILC 2的缺失导致VAT嗜酸性粒细胞和AAM的显著减少，并且还损害了感染巴西日本圆线虫后VAT嗜酸性粒细胞的扩增，巴西日本圆线虫是一种与脂肪ILC 2细胞因子产生增加和胰岛素敏感性增强相关的肠道寄生虫。此外，IL-33（先前显示促进ILC 2产生细胞因子的细胞因子）导致VAT嗜酸性粒细胞和AAM的快速ILC 2依赖性增加。因此，ILC 2驻留在VAT中并促进嗜酸性粒细胞和AAM参与代谢稳态，并且该轴在Th 2相关免疫刺激期间增强。
Innate lymphoid type 2 cells maintain eosinophils and alternatively activated macrophages in visceral fat via the production of IL-5 and IL-13. Eosinophils in visceral adipose tissue (VAT) have been implicated in metabolic homeostasis and the maintenance of alternatively activated macrophages (AAMs). The absence of eosinophils can lead to adiposity and systemic insulin resistance in experimental animals, but what maintains eosinophils in adipose tissue is unknown. We show that interleukin-5 (IL-5) deficiency profoundly impairs VAT eosinophil accumulation and results in increased adiposity and insulin resistance when animals are placed on a high-fat diet. Innate lymphoid type 2 cells (ILC2s) are resident in VAT and are the major source of IL-5 and IL-13, which promote the accumulation of eosinophils and AAM. Deletion of ILC2s causes significant reductions in VAT eosinophils and AAMs, and also impairs the expansion of VAT eosinophils after infection with Nippostrongylus brasiliensis, an intestinal parasite associated with increased adipose ILC2 cytokine production and enhanced insulin sensitivity. Further, IL-33, a cytokine previously shown to promote cytokine production by ILC2s, leads to rapid ILC2-dependent increases in VAT eosinophils and AAMs. Thus, ILC2s are resident in VAT and promote eosinophils and AAM implicated in metabolic homeostasis, and this axis is enhanced during Th2-associated immune stimulation.
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