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Publication Detail

Title: Costimulation of type-2 innate lymphoid cells by GITR promotes effector function and ameliorates type 2 diabetes.

Authors: Galle-Treger, Lauriane; Sankaranarayanan, Ishwarya; Hurrell, Benjamin P; Howard, Emily; Lo, Richard; Maazi, Hadi; Lewis, Gavin; Banie, Homayon; Epstein, Alan L; Hu, Peisheng; Rehan, Virender K; Gilliland, Frank D; Allayee, Hooman; Soroosh, Pejman; Sharpe, Arlene H; Akbari, Omid

Published In Nat Commun, (2019 02 12)

Abstract: 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.

PubMed ID: 30755607 Exiting the NIEHS site

MeSH Terms: Adipose Tissue/immunology; Adipose Tissue/metabolism; Animals; Cytokines/immunology; Cytokines/metabolism; Diabetes Mellitus, Type 2/immunology*; Diabetes Mellitus, Type 2/metabolism; Glucocorticoid-Induced TNFR-Related Protein/immunology*; Glucocorticoid-Induced TNFR-Related Protein/metabolism; Glucose/metabolism; Homeostasis; Humans; Immunity, Innate; Insulin Resistance; Lymphocytes/immunology*; Lymphocytes/metabolism*; Mice; Mice, Inbred C57BL; Mice, Knockout; Th2 Cells/metabolism

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