Dendritic cells and adipose tissue

Abstract

Visceral adipose tissue inflammation in obesity is an established risk factor for metabolic syndrome, which can include insulin resistance, type 2 diabetes, hypertension and cardiovascular diseases. With obesity and related metabolic disorders reaching epidemic proportions globally, an understanding of the mechanisms of adipose tissue inflammation is crucial. Within the immune cell cohort, dendritic cells (DC) play a key role in balancing tolerance and immunity. Despite decades of research into the characterization of DC in lymphoid and non-lymphoid organs, their role in adipose tissue function is poorly understood. There is now an increasing interest in identification and characterization of DC in adipose tissue and understanding their function in regulating tissue metabolic homeostasis. This review provides an overview of the study of DC in adipose tissue, focusing on possible mechanisms by which DC may contribute to adipose tissue homeostasis.

Keywords: adipose tissue; dendritic cells; inflammation; metabolism; obesity.

Figure 1

Schematic showing the potential response of stimulated adipose tissue dendritic cells (AT DC). Once activated, DC within AT may migrate along the lymphatic system (shown in green) to mesenteric lymph nodes (mLN) to activate naive T cells and bring about T‐cell responses [T helper type 17 and type 1 (Th17/Th1)].

Figure 2

Schematic depicting adipose tissue homeostasis and its response in obesity. Under normal/lean conditions, immune cells and adipocytes work in cooperation to develop a tolerogenic milieu to maintain tissue homeostasis. In response to obesity‐induced chronic inflammation, immune cells including dendritic cells (DC) and macrophages are recruited to adipose tissue, promoting a pro‐inflammatory response. Dotted black arrows indicate possible transcriptional and systemic regulation of DC, which may result in anti‐ or pro‐inflammatory responses. HIF‐1α, hypoxia‐inducible factor‐1α; KLF4, Kruppel‐like factor 4; IL‐4, interleukin‐4; PPARγ, peroxisome proliferator‐activated receptor γ; TGF‐β, transforming growth factor‐β; TNF‐α, tumour necrosis factor‐α.