Unusual Suspects in the Development of Obesity-Induced Inflammation and Insulin Resistance: NK cells, iNKT cells, and ILCs.

Unusual Suspects in the Development of Obesity-Induced Inflammation and Insulin Resistance: NK cells, iNKT cells, and ILCs.
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DOI:
10.4093/dmj.2017.41.4.229
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发表时间:
2017-08
影响因子:
5.9
通讯作者:
Lee J
Lee J
中科院分区:
医学2区
文献类型:
--
作者:
Bonamichi BDSF;Lee J

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在动物模型和人类中,肥胖诱导的炎症介导胰岛素抵抗的发展这一观点得到了强有力的支持。还已经显示,局部组织中的免疫细胞,特别是内脏脂肪组织中的免疫细胞,在肥胖诱导的炎症的调节中起主要作用。具体而言,肥胖增加促炎免疫细胞的数量和活化,包括M1巨噬细胞、嗜中性粒细胞、Th1 CD4 T细胞和CD8 T细胞,同时抑制抗炎细胞,如M2巨噬细胞、CD4调节性T细胞、调节性B细胞和嗜酸性粒细胞。然而,最近,新的细胞类型已被证明参与肥胖诱导的炎症和胰岛素抵抗的发展。其中一些细胞类型似乎也可以调节肥胖。这些细胞是自然杀伤(NK)细胞和先天淋巴细胞(ILC),它们是密切相关的,并且是不变的自然杀伤T(iNKT)细胞。值得注意的是,虽然iNKT细胞在名称上类似于NK细胞,但就其在免疫和代谢中的发育和功能而言,它们实际上是完全不同的细胞类型。在这篇综述中,我们将重点介绍这些相对较新的参与者在代谢领域发挥的作用,肥胖诱导的胰岛素抵抗和肥胖的调节。
The notion that obesity-induced inflammation mediates the development of insulin resistance in animal models and humans has been gaining strong support. It has also been shown that immune cells in local tissues, in particular in visceral adipose tissue, play a major role in the regulation of obesity-induced inflammation. Specifically, obesity increases the numbers and activation of proinflammatory immune cells, including M1 macrophages, neutrophils, Th1 CD4 T cells, and CD8 T cells, while simultaneously suppressing anti-inflammatory cells such as M2 macrophages, CD4 regulatory T cells, regulatory B cells, and eosinophils. Recently, however, new cell types have been shown to participate in the development of obesity-induced inflammation and insulin resistance. Some of these cell types also appear to regulate obesity. These cells are natural killer (NK) cells and innate lymphoid cells (ILCs), which are closely related, and invariant natural killer T (iNKT) cells. It should be noted that, although iNKT cells resemble NK cells in name, they are actually a completely different cell type in terms of their development and functions in immunity and metabolism. In this review, we will focus on the roles that these relatively new players in the metabolism field play in obesity-induced insulin resistance and the regulation of obesity.
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