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Publication : Insulin Receptor-Mediated Stimulation Boosts T Cell Immunity during Inflammation and Infection.

First Author  Tsai S Year  2018
Journal  Cell Metab Volume  28
Issue  6 Pages  922-934.e4
PubMed ID  30174303 Mgi Jnum  J:269126
Mgi Id  MGI:6270090 Doi  10.1016/j.cmet.2018.08.003
Citation  Tsai S, et al. (2018) Insulin Receptor-Mediated Stimulation Boosts T Cell Immunity during Inflammation and Infection. Cell Metab 28(6):922-934.e4
abstractText  T cells represent a critical effector of cell-mediated immunity. Activated T cells engage in metabolic reprogramming during effector differentiation to accommodate dynamic changes in energy demands. Here, we show that the hormone, insulin, and downstream signaling through its insulin receptor shape adaptive immune function through modulating T cell metabolism. T cells lacking insulin receptor expression (LckCre+ Insr(fl/fl)) show reduced antigen-specific proliferation and compromised production of pro-inflammatory cytokines. In vivo, T cell-specific insulin receptor deficiency reduces T cell-driven colonic inflammation. In a model of severe influenza infection with A/PR8 (H1N1), lack of insulin receptor on T cells curtails antigen-specific immunity to influenza viral antigens. Mechanistically, insulin receptor signaling reinforces a metabolic program that supports T cell nutrient uptake and associated glycolytic and respiratory capacities. These data highlight insulin receptor signaling as an important node integrating immunometabolic pathways to drive optimal T cell effector function in health and disease.
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