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Costimulation of type-2 innate lymphoid cells by GITR promotes effector function and ameliorates type 2 diabetes
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Costimulation of type-2 innate lymphoid cells by GITR promotes effector function and ameliorates type 2 diabetes
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Journal Article
Costimulation of type-2 innate lymphoid cells by GITR promotes effector function and ameliorates type 2 diabetes
2019
Overview
Metabolic syndrome is characterized by disturbances in glucose homeostasis and the development of low-grade systemic inflammation, which increase the risk to develop type 2 diabetes mellitus (T2DM). Type-2 innate lymphoid cells (ILC2s) are a recently discovered immune population secreting Th2 cytokines. While previous studies show how ILC2s can play a critical role in the regulation of metabolic homeostasis in the adipose tissue, a therapeutic target capable of modulating ILC2 activation has yet to be identified. Here, we show that GITR, a member of the TNF superfamily, is expressed on both murine and human ILC2s. Strikingly, we demonstrate that GITR engagement of activated, but not naïve, ILC2s improves glucose homeostasis, resulting in both protection against insulin resistance onset and amelioration of established insulin- resistance. Together, these results highlight the critical role of GITR as a novel therapeutic molecule against T2DM and its fundamental role as an immune checkpoint for activated ILC2s.
Type-2 innate lymphoid cells (ILC2s) are an immune population secreting Th2 cytokines playing a role in the regulation of adipose metabolic homeostasis. Here the authors show that engagement of GITR, a member of the TNF superfamily, in activated ILC2s is protective against insulin resistance in both a preventive and a therapeutic manner in the context of obesity.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 14/63
/ 82/1
/ 82/51
/ 82/80
/ Animals
/ Diabetes
/ Diabetes mellitus (non-insulin dependent)
/ Diabetes Mellitus, Type 2 - immunology
/ Diabetes Mellitus, Type 2 - metabolism
/ Glucocorticoid-Induced TNFR-Related Protein - immunology
/ Glucocorticoid-Induced TNFR-Related Protein - metabolism
/ Glucose
/ Humanities and Social Sciences
/ Humans
/ Insulin
/ Mice
/ Science
