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Unusual Suspects in the Development of Obesity-Induced Inflammation and Insulin
Resistance: NK cells, iNKT cells, and ILCs
#MMPMID28537058
Bonamichi BDSF
; Lee J
Diabetes Metab J
2017[Aug]; 41
(4
): 229-250
PMID28537058
show ga
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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