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γδ T cells and adipocyte IL-17RC control fat innervation and thermogenesis
γδ T cells and adipocyte IL-17RC control fat innervation and thermogenesis
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γδ T cells and adipocyte IL-17RC control fat innervation and thermogenesis
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γδ T cells and adipocyte IL-17RC control fat innervation and thermogenesis
γδ T cells and adipocyte IL-17RC control fat innervation and thermogenesis

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γδ T cells and adipocyte IL-17RC control fat innervation and thermogenesis
γδ T cells and adipocyte IL-17RC control fat innervation and thermogenesis
Journal Article

γδ T cells and adipocyte IL-17RC control fat innervation and thermogenesis

2020
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Overview
The sympathetic nervous system innervates peripheral organs to regulate their function and maintain homeostasis, whereas target cells also produce neurotrophic factors to promote sympathetic innervation 1 , 2 . The molecular basis of this bi-directional communication remains to be fully determined. Here we use thermogenic adipose tissue from mice as a model system to show that T cells, specifically γδ T cells, have a crucial role in promoting sympathetic innervation, at least in part by driving the expression of TGFβ1 in parenchymal cells via the IL-17 receptor C (IL-17RC). Ablation of IL-17RC specifically in adipose tissue reduces expression of TGFβ1 in adipocytes, impairs local sympathetic innervation and causes obesity and other metabolic phenotypes that are consistent with defective thermogenesis; innervation can be fully rescued by restoring TGFβ1 expression. Ablating γδ Τ cells and the IL-17RC signalling pathway also impairs sympathetic innervation in other tissues such as salivary glands. These findings demonstrate coordination between T cells and parenchymal cells to regulate sympathetic innervation. Vγ6 + Vδ1 + γδ T cells control tolerance to cold by activating adipocyte IL-17RC and promoting sympathetic innervation of thermogenic adipose tissue in mice.