中国免疫学杂志2024,Vol.40Issue(4) :832-839.DOI:10.3969/j.issn.1000-484X.2024.04.028

代谢"废物"乳酸在肿瘤微环境中的免疫抑制作用

Immunosuppressive effect of metabolic"waste"lactic acid in tumor microenvironment

苑思羽 侯俊杰 张片红
中国免疫学杂志2024,Vol.40Issue(4) :832-839.DOI:10.3969/j.issn.1000-484X.2024.04.028

代谢"废物"乳酸在肿瘤微环境中的免疫抑制作用

Immunosuppressive effect of metabolic"waste"lactic acid in tumor microenvironment

苑思羽 1侯俊杰 2张片红1
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作者信息

  • 1. 浙江大学医学院附属第二医院营养科,杭州 310009
  • 2. 吉林省人民医院肿瘤综合治疗科,长春 130021
  • 折叠

摘要

近年来,肿瘤微环境(TME)备受科学家们的关注,它是由肿瘤细胞、肿瘤相关成纤维细胞(CAFs)、免疫细胞、血管、细胞外基质、周围支持组织及其所在的代谢环境等共同组成的复杂体系.免疫逃逸和代谢改变(葡萄糖有氧代谢转至无氧代谢产生乳酸)是此体系的两个基本特征.虽然过去一直认为乳酸是TME中的代谢废物,但现在人们普遍认为乳酸的增加和TME的酸化在肿瘤发生发展中发挥关键作用,包括免疫逃逸、组织侵袭/肿瘤转移、血管生成和肿瘤耐药等.因此,研究TME中乳酸代谢、免疫抑制、血管生成、肿瘤耐药等关键过程的调控机制,可为靶向TME的新治疗策略提供理论基础和实践依据.

Abstract

In recent years,the tumor microenvironment(TME)has garnered significant attention from scientists.It is a com-plex system composed of tumor cells,cancer-associated fibroblasts(CAFs),immune cells,blood vessels,extracellular matrix,sur-rounding supportive tissues and their metabolic environment.Two fundamental characteristics of this system are immune escape and metabolic changes(the shift from aerobic to anaerobic metabolism of glucose,leading to lactate production).Although lactate has tra-ditionally been considered a metabolic"waste"product in the TME,it is now widely recognized that the increase in lactate and the acidification of the tumor microenvironment play key roles in tumor development and progression,including immune escape,tissue in-vasion/tumor metastasis,angiogenesis and tumor drug resistance.Therefore,studying the regulatory mechanisms of lactate metabo-lism,immune suppression,angiogenesis,and tumor drug resistance in the TME can provide a theoretical basis and practical evidence for new therapeutic strategies targeting the TME.

关键词

乳酸代谢/免疫抑制/肿瘤微环境

Key words

Lactic acid metabolism/Immunosuppressive/Tumor microenvironment

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基金项目

吉林省科技发展计划项目(20230402007GH)

出版年

2024
中国免疫学杂志
中国免疫学会,吉林省医学期刊社

中国免疫学杂志

CSTPCDCSCD北大核心
影响因子:0.926
ISSN:1000-484X
参考文献量96
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