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Regulation of Type 2 Innate Lymphoid Cells in the adipose tissue

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Innate lymphoid cells (ILCs) are a lymphocyte subset which lack adaptive antigen-specific receptors, being the innate counterparts of T helper lymphocytes. ILCs act early in the immune response by producing effector cytokines in response to tissue-derived inducer cytokines. ILC2s, a subtype of ILCs, produce type 2 cytokines in response to helminthic infection, allergens, and epithelial injury. Besides their role in immune defense, ILC2s also contribute to metabolic homeostasis by maintaining an anti-inflammatory protective environment in the adipose tissue (AT). In obesity, excessive lipid accumulation results in chronic low-grade inflammation, causing a shift in immune cell populations that can lead to a systemic metabolic imbalance, known as metabolic syndrome. ILC2-derived molecules act on immune cells and on adipocytes, limiting obesity-induced inflammation and lipid accumulation, respectively. However, how ILC2s perceive environmental cues and integrate signals to maintain AT homeostasis remains poorly understood. Here, we hypothesize that neuroimmune interactions can control ILC2 function in the AT downstream from sympathetic nervous system innervation. Using pharmacological, genetic and imaging approaches, we show that AT ILC2s can integrate neuroregulatory molecules to control AT physiology.

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Obesity adipose tissue type 2 innate lymphoid cells neuroimmune interactions

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