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瘤相关巨细胞的NAMPT驱动的M2极化导致结肠直肠癌中的免疫抑制微环境

Sun Mi Hong¹, A-Yeon Lee^1,2, Byeong-Ju Kim^1,2

¹Department of Biochemistry, Ajou University School of Medicine, 164 Worldcup-ro, Yeongtong-gu, Suwon, Gyeonggi-do, 16499, Republic of Korea.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

|February 2, 2024

概括

在与瘤相关的巨细胞中,尼古丁胺胺酸基转移酶 (NAMPT) 通过抑制抗瘤免疫力,促进结直肠癌的进展. 针对NAMPT可能会扭转这种情况,创造一个免疫刺激性瘤微环境,以改善患者的治疗结果.

科学领域:

免疫学免疫学免疫学
在瘤学瘤学.
代谢酶是代谢酶中的一种.

背景情况:

尼古丁胺酸转移酶 (NAMPT) 在炎症中至关重要,但其在结直肠癌 (CRC) 瘤微环境 (TME) 细胞中的作用尚未得到研究.
在CRC中,NAMPT在免疫抑制性SPP1+瘤相关巨细胞 (TAMs) 中高度表达.
在这些TAM中,高NAMPT基因特征与患者预后不佳相关.

研究的目的:

调查NAMPT在结直肠癌发育过程中的髓状细胞中的作用.
探索NAMPT缺陷对TAM两极化和功能的影响.
评估在CRC中针对NAMPT的治疗潜力.

主要方法:

单细胞RNA测序 (scRNA-seq) 对CRC TME的分析.
在CRC过程中,在小鼠的髓状体内遗传删除Nampt.
评估巨细胞极化,细胞和免疫信号通路 (HIF-1α,STING,I型IFN).
在TME中分析细胞毒性T细胞活性.

主要成果:

巨细胞中的NAMPT缺陷破坏了HIF-1α的稳定,减少了类似M2的TAM两极分化.
巨细胞NAMPT缺陷降低了细胞分裂,增强了STING信号传递和I型IFN反应.
这些免疫反应通过强化细胞毒性T细胞活性来促进抗瘤免疫力.

结论:

在SPP1+TAM中NAMPT表达预测CRC结果不佳.
在TAM中准NAMPT可以将TME重新编程到免疫刺激状态.
针对NAMPT的策略为CRC治疗提供了潜在的治疗途径.

关键词:

在CRC中,CRC就是CRC.这就是HIF-1α.像M2这样的TAM.这个名字叫做NAMPT.刺痛是一种刺痛.

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