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γδ T 细胞和脂肪细胞 IL-17RC 控制脂肪内化和热生成

Bo Hu^1,2, Chengcheng Jin^3,4, Xing Zeng^1,2

¹Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA, USA.

|February 21, 2020

概括

T细胞,特别是三角T细胞,对交感神经系统内化至关重要,部分是通过影响TGFβ1的表达. 这一发现揭示了神经与目标细胞之间的双向通信.

科学领域:

免疫学
神经科学
代谢研究

背景情况:

交感神经系统调节器官功能和平衡.
目标细胞和交感神经之间的双向通信是必不可少的,但尚未完全理解.
目标细胞产生的神经损伤因子促进交感内置.

研究的目的:

阐明交感内置的分子机制.
研究T细胞在调节交感内置中的作用.
在脂肪组织和其他器官中探索玛三角T细胞和IL-17RC的功能.

主要方法:

使用来自小鼠的热生成脂肪组织作为模型系统.
研究了马三角形T细胞和IL-17RC信号通路的作用.
研究了在脂肪组织中消去IL-17RC对TGFβ1表达,交感内置和代谢表型的影响.
在切除 gamma delta T 细胞和 IL- 17RC 后,评估了唾液腺的交感内化.

主要成果:

通过通过IL-17RC驱动TGFβ1表达,加玛三角型T细胞促进交感内置.
在脂肪组织中切除IL-17RC会减少TGFβ1的表达,损害交感内置,并导致肥胖和代谢功能障碍.
恢复TGFβ1表达完全挽救了内化缺陷.
在抹去 gamma delta T 细胞和 IL- 17RC 时,还观察到唾液腺体的交感内置受损.

结论:

T细胞,特别是玛特拉T细胞,在调节交感内方面发挥着至关重要的作用.
IL-17RC通路和TGFβ1是T细胞与辅酶细胞之间控制交感内置的关键介质.
这些发现揭示了免疫系统和神经系统之间维持组织平衡和代谢健康的新协调机制.

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