小柯机器人

γδT细胞和脂肪细胞调控脂肪神经支配和产热
2020-02-29 23:40

美国丹娜—法伯癌症研究所Bruce M. Spiegelman小组近日取得一项新成果。他们发现γδ T细胞和脂肪细胞IL-17RC调控脂肪神经支配和产热。2020年2月19日出版的《自然》在线发表了这项成果。

研究人员利用小鼠产热脂肪组织作为模型系统,发现T细胞(尤其是γδ T细胞)在促进交感神经支配方面发挥关键作用,至少部分是通过经由IL-17受体C(IL-17RC)驱动TGFβ1在实质细胞中表达来完成的。特别是在脂肪组织中IL-17RC缺失会降低脂肪细胞中TGFβ1的表达、损害局部交感神经、并导致肥胖和其他代谢表型,这与产热不良的表型类似。

通过恢复TGFβ1的表达,神经支配可以得到完全挽救。γδ T细胞和IL-17RC信号同时缺失也损害了其他组织如唾液腺的交感神经。这些发现表明T细胞和实质细胞之间相协调以调控交感神经支配。

据悉,交感神经系统支配周围器官以调节其功能并维持体内稳态,而靶细胞也产生神经营养因子以促进交感神经支配。人们尚不完全清楚这种双向交流的分子基础。

附:英文原文

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

Author: Bo Hu, Chengcheng Jin, Xing Zeng, Jon M. Resch, Mark P. Jedrychowski, Zongfang Yang, Bhavna N. Desai, Alexander S. Banks, Bradford B. Lowell, Diane Mathis, Bruce M. Spiegelman

Issue&Volume: 2020-02-19

Abstract: The sympathetic nervous system innervates peripheral organs to regulate their function and maintain homeostasis, whereas target cells also produce neurotrophic factors to promote sympathetic innervation1,2. 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.

DOI: 10.1038/s41586-020-2028-z

Source: https://www.nature.com/articles/s41586-020-2028-z

Nature:《自然》,创刊于1869年。隶属于施普林格·自然出版集团,最新IF:43.07
官方网址:http://www.nature.com/
投稿链接:http://www.nature.com/authors/submit_manuscript.html


本期文章:《自然》:Online/在线发表

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