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25-基胆固醇调节溶酶体AMP激酶激活和代谢重编程,以教育免疫抑制性巨细胞

Jun Xiao¹, Shuang Wang², Longlong Chen³

¹Key Laboratory of RNA Science and Engineering, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai 200031, China; Department of Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong, China.

|April 19, 2024

概括

胆固醇-25-基酶 (Ch25h) 在瘤中促进免疫抑制性巨细胞. 抑制Ch25h可以增强抗瘤免疫力和T细胞活性,提供一个新的治疗点.

科学领域:

免疫学免疫学免疫学
癌症生物学癌症生物学
代谢途径代谢途径

背景情况:

巨细胞是将"冷"瘤转化为免疫性"热"瘤的关键.
瘤微环境 (TME) 中的改变胆固醇代谢物具有未知的作用.
胆固醇-25-基酶 (Ch25h) 和它的产物25-基胆固醇 (25HC) 有关.

研究的目的:

阐明25h和25HC在TME中的功能.
为了研究Ch25h在巨细胞免疫抑制中的作用.
探索Ch25h作为癌症免疫治疗中的潜在治疗标.

主要方法:

单细胞RNA测序 (scRNA-seq) 用于识别表达CH25H的巨细胞子集.
在体外和体外实验以准Ch25h并评估其对巨细胞功能和抗瘤免疫力的影响.
涉及溶酶体通路,G蛋白结合受体155 (GPR155),哺乳动物目标拉巴胺复合物1 (mTORC1) 和AMP激活蛋白激酶α (AMPKα) 的机制研究.

主要成果:

互白素-4 (IL-4) 和IL-13通过STAT6诱导Ch25h的表达,导致25HC的积累.
巨细胞中高CH25H表达与免疫抑制和各种癌症的生存率差相关.
向Ch25h减少了巨细胞的免疫抑制,增加了T细胞的透和激活,并与抗PD-1疗法产生协同作用.
25HC积累抑制了mTORC1通过GPR155传递信号,从而激活AMPKα.
AMPKα的激活会重编程巨细胞代谢,并增强STAT6的激活,从而促进阿基因酶1 (ARG1) 的产生.

结论:

Ch25h 作为癌症中的免疫代谢检查点.
Ch25h操纵巨细胞的表型,以抑制抗瘤CD8+T细胞的反应.
向Ch25h代表了增强癌症免疫治疗的有希望的策略.

关键词:

25氧胆固醇是25-氧胆固醇的一种.这就是AMPKK.CH25H 是一种酸盐.类似M2的巨细胞.在STAT6中,胆固醇的代谢过程氧化胆固醇是一种氧化醇.瘤免疫疗法免疫疗法与瘤相关的巨细胞.

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