Abstract
Type 2 innate lymphoid cells (ILC2) are the innate counterparts of Th2 cells and are critically involved in the maintenance of homeostasis in a variety of tissues. Instead of expressing specific antigen receptors, ILC2s respond to external stimuli such as alarmins released from damage. These cells help control the delicate balance of inflammation in adipose tissue, which is a determinant of metabolic outcome. ILC2s play a key role in the pathogenesis of type 2 diabetes mellitus (T2DM) through their protective effects on tissue homeostasis. A variety of crosstalk takes place between resident adipose cells and ILC2s, with each interaction playing a key role in controlling this balance. ILC2 effector function is associated with increased browning of adipose tissue and an anti-inflammatory immune profile. Trafficking and maintenance of ILC2 populations are critical for tissue homeostasis. The metabolic environment and energy source significantly affect the number and function of ILC2s in addition to affecting their interactions with resident cell types. How ILC2s react to changes in the metabolic environment is a clear determinant of the severity of disease. Treating sources of metabolic instability via critical immune cells provides a clear avenue for modulation of systemic homeostasis and new treatments of T2DM.
Highlights
Type 2 diabetes mellitus (T2DM) is a disease characterized by the inability to maintain healthy glucose levels due to systemic insulin resistance
Their maintenance of homeostasis and healthy tissue growth in the presence of a highfat diet (HFD) and obesity is mediated by their support of antiinflammatory adipose tissue macrophages (ATM) populations [18, 19, 47, 48]
Beyond their direct effects on systemic homeostasis, how ILC2s fight harmful inflammation in a variety of contexts will be described here as their direct regulation of a changing adipose environment is key in the prevention of type 2 diabetes mellitus (T2DM) and possible future treatments
Summary
Type 2 diabetes mellitus (T2DM) is a disease characterized by the inability to maintain healthy glucose levels due to systemic insulin resistance. Activation of ILC2s has been shown to increase the expression of genes associated with higher metabolism including genes for mitochondrial chain complexes I (Nd1 and Nd2), III (Cytb), IV (Cox1a), V (Atp6), and tyrosine hydroxylase in VAT lysates [28] Their maintenance of homeostasis and healthy tissue growth in the presence of a highfat diet (HFD) and obesity is mediated by their support of antiinflammatory ATM populations [18, 19, 47, 48]. Chronic release of the cytokine in cases of obesity and other conditions leads to effects in adipose tissue, pancreas, liver, and muscle [51] Beyond their direct effects on systemic homeostasis, how ILC2s fight harmful inflammation in a variety of contexts will be described here as their direct regulation of a changing adipose environment is key in the prevention of T2DM and possible future treatments. Overall, maintaining homeostasis in VAT is essential to preventing systemic metabolic syndrome and insulin resistance
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