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Abstract
Evidence accumulated over the past few years has documented a critical role for adipose tissue (AT)-resident immune cells in the regulation of local and systemic metabolic homeostasis. In the lean state, visceral adipose tissue (VAT) is predominated by anti-inflammatory T-helper 2 (Th2) and regulatory T (Treg) cell subsets. As obesity progresses, the population of Th2 and Treg cells decreases while that of the T-helper 1 (Th1) and T-helper 17 (Th17) cells increases, leading to augmented inflammation and insulin resistance. Notably, recent studies also suggest a potential role of CD4+ T cells in the control of thermogenesis and energy homeostasis. In this review, we have summarized recent advances in understanding the characteristics and functional roles of AT CD4+ T cell subsets during obesity and energy expenditure. We have also discussed new findings on the crosstalk between CD4+ T cells and local antigen-presenting cells (APCs) including adipocytes, macrophages, and dendritic cells (DCs) to regulate AT function and metabolic homeostasis. Finally, we have highlighted the therapeutic potential of targeting CD4+ T cells as an effective strategy for the treatment of obesity and its associated metabolic diseases.
Highlights
Obesity, which is associated with various metabolic and cardiovascular diseases such as insulin resistance, type 2 diabetes, hypertension, and stroke, is among the most severe health threats to modern society [1, 2]
While the role of Adipose Tissue Macrophages (ATMs) in adipose tissue (AT) inflammation is well documented, several studies report that macrophages do not infiltrate into AT until 10 weeks after HFD feeding [7, 42]
Several studies report that macrophages do not infiltrate into AT until 10 weeks after HFD feeding while major histocompatibility complex (MHCII) family genes are upregulated at 2 weeks after HFD, indicating that adipocytes but not ATMs are the antigenpresenting cells (APCs) that initiate T cells
Summary
Obesity, which is associated with various metabolic and cardiovascular diseases such as insulin resistance, type 2 diabetes, hypertension, and stroke, is among the most severe health threats to modern society [1, 2]. It is suggested that, as obesity advances, leptin secreted by adipocytes stimulates IFN-γ production from CD4+ T cells, which further promotes adipocyte MHCII expression and Th1 differentiation, leading to a vicious cycle of AT inflammation [42].
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