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在调节性T细胞中,乳酸驱动的TNFR2表达促进了恶性多流的进展

Qianqian Xue¹, Wenbei Peng¹, Siyu Zhang¹

¹Department of Respiratory and Critical Care Medicine, Huazhong University of Science and Technology, Wuhan, China.

Journal for immunotherapy of cancer

|December 25, 2024

概括

乳酸上调调节调节性T细胞 (Treg细胞) 上的瘤缩因子受体2 (TNFR2),增强恶性多流液 (MPE) 中的免疫抑制. 与免疫检查点阻塞 (ICB) 一起准乳酸代谢,可以提高MPE治疗的疗效.

科学领域:

免疫学免疫学免疫学
癌症生物学癌症生物学
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.

背景情况:

瘤亡因子受体2 (TNFR2) 是癌症免疫治疗的目标.
调控TNFR2基因表达及其对瘤透调控T细胞 (Treg细胞) 的影响尚不清楚.

研究的目的:

研究调节Treg细胞TNFR2表达的因素.
阐明TNFR2和乳酸在恶性多发性溢血 (MPE) 进展中的作用.
探索针对MPE治疗的Treg细胞中乳酸代谢的治疗策略.

主要方法:

单细胞RNA测序以比较TNFR2+和TNFR2-Treg细胞.
使用了人类和小鼠恶性多叶流液 (MPE) 模型.
研究了乳酸通过基因素乳化 (H3K18la) 和NF-κB p65.5调节TNFR2表达的作用.

主要成果:

在Treg细胞上高TNFR2表达与MPE预后不佳和免疫检查点分子升高相关.
乳酸上调调节Treg细胞上的TNFR2,增加MPE中的免疫抑制.
乳酸代谢阻断结合免疫检查点阻断 (ICB) 疗法改善了小鼠的MPE治疗结果.

结论:

发现了MPE中Treg细胞TNFR2调节的机制,涉及乳酸和表观遗传修饰 (H3K18la).
突出了乳酸驱动的TNFR2表达在MPE进展中的作用.
建议将Treg细胞中的乳酸代谢作为MPE潜在的治疗策略.

关键词:

免疫治疗是一种免疫疗法.肺癌肺癌是一种肺癌.一个T调节单元 - Treg调节单元瘤微环境 - - 瘤微环境

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