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高细胞外K+偏向T细胞对瘤的分化促进Th2和Treg子集

Brandon Han Siang Wong^1,2, Zhi Sheng Poh¹, James Tan Chia Wei¹

¹Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore, Singapore.

European journal of immunology

|December 9, 2024

概括

死亡瘤细胞中的高细胞外 (K+) 通过减少关键受体和改变新陈代谢,损害T细胞功能. 这通过抑制瘤微环境 (TME) 内的抗瘤T细胞反应来促进瘤生长.

科学领域:

免疫学免疫学免疫学
癌症生物学癌症生物学
细胞生理学细胞生理学

背景情况:

死亡的瘤细胞释放离子 (K+),在瘤微环境 (TME) 中增加细胞外K+度 ([K+]e).
升高的[K+]e与免疫抑制性TME有关,但其对T细胞功能的直接影响尚未完全阐明.

研究的目的:

研究高细胞外 ([K+]e) 对T细胞受体信号传递,新陈代谢和分化的影响.
了解[K+]e如何促进肝细胞癌 (HCC) 和结直肠癌 (CRC) 中的免疫抑制性TME.

主要方法:

分析T细胞受体子单元表达 (CD3ε,CD3ζ) 和共刺激受体CD28.
评估T细胞代谢概况,包括葡萄糖和谷氨酸代谢.
流细胞计和GeoMx数字空间分析分析瘤组织中的T细胞表型.

主要成果:

高[K+]e显著降低了T细胞上的CD3ε,CD3ζ和CD28表达.
升高的[K+]e改变了T细胞代谢,限制了葡萄糖和谷氨酸的利用,表明功能疲劳.
高[K+]e倾斜T细胞分化向促进瘤的Th2和调节性T (iTreg) 细胞,同时抑制抗瘤的Th1和Th17细胞.

结论:

高细胞外度是调节T细胞功能和促进免疫抑制瘤微环境的关键因素.
这些发现揭示了一种新的机制,瘤细胞死亡有助于免疫逃避和瘤进展.
向细胞外水平可能是增强抗瘤免疫力的潜在治疗策略.

关键词:

T细胞耗尽的情况的T-淋巴细胞.免疫抑制免疫抑制代谢生物组的代谢生物组

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