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通过依赖谷氨酸酶的新陈代谢明显调节Th17和Th1细胞的分化

Marc O Johnson¹, Melissa M Wolf², Matthew Z Madden²

¹Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA; Department of Pharmacology and Cancer Biology, Duke University, Durham, NC 27710, USA.

|November 6, 2018

概括

谷氨酸酶 (GLS) 对T细胞的激活和分化至关重要. 它的缺陷会损害Th17细胞,但会增强CD4 Th1和CD8 CTL细胞,显示T细胞代谢编程中的不同作用.

科学领域:

免疫学
细胞代谢
分子生物学

背景情况:

激活的T细胞表现出其功能所必需的多种代谢程序.
谷氨酸酶 (GLS) 是谷氨酸代谢中的关键酶,支持细胞过程,如三碳酸循环,氧化还原平衡和表观遗传修饰.

研究的目的:

研究谷氨酸酶 (GLS) 在T细胞激活,分化和效应器功能中的作用.
阐明GLS介导的谷氨酸代谢如何影响不同的T细胞子集,包括Th17,Th1和CD8CTL细胞.

主要方法:

在GLS缺陷模型中分析T细胞激活,增殖和分化.
评估T细胞中的基因表达和染色质可访问性变化.
使用GLS无T细胞进行体内研究,以评估它们在炎症疾病中的作用.
对T细胞群的短暂GLS抑制的评估.

主要成果:

导致T细胞活化和增殖的降低,从而损害了Th17细胞的分化.
GLS的丧失增强了Tbet表达,促进了CD4 Th1和CD8 CTL细胞的分化和效应功能.
在GLS缺乏的T细胞中观察到染色体可及性和基因表达的改变,包括Th1细胞PIK3IP1的降低.
在体内,GLS无T细胞未能诱导Th17驱动的炎症,而Th1细胞最初显示功能增强,但最终被耗尽.
暂时的GLS抑制增加了Th1和CTLT细胞数量.

结论:

由GLS调节的谷氨酸代谢在促进Th17细胞分化的过程中发挥着独特的作用,同时限制了Th1和CTL效应细胞的发展.
针对GLS可以提供一种策略来调节T细胞子集的分化,用于免疫相关疾病的治疗干预.

关键词:

一个T细胞染色体葡萄糖胺酶氨酸在 mTOR 代谢过程

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