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肿瘤相关巨噬细胞在胶质瘤微环境中的募集机制及治疗意义。

Recruitment mechanisms and therapeutic implications of tumor-associated macrophages in the glioma microenvironment.

机构信息

Brain Tumor Research Center, Beijing Neurosurgical Institute, Beijing Laboratory of Biomedical Materials, Beijing, China.

出版信息

Front Immunol. 2023 Apr 20;14:1067641. doi: 10.3389/fimmu.2023.1067641. eCollection 2023.

DOI:10.3389/fimmu.2023.1067641
PMID:37153567
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10157099/
Abstract

As one of the main components of the glioma immune microenvironment, glioma-associated macrophages (GAMs) have increasingly drawn research interest. Primarily comprised of resident microglias and peripherally derived mononuclear macrophages, GAMs are influential in a variety of activities such as tumor cell resistance to chemotherapy and radiotherapy as well as facilitation of glioma pathogenesis. In addition to in-depth research of GAM polarization, study of mechanisms relevant in tumor microenvironment recruitment has gradually increased. Suppression of GAMs at their source is likely to produce superior therapeutic outcomes. Here, we summarize the origin and recruitment mechanism of GAMs, as well as the therapeutic implications of GAM inhibition, to facilitate future glioma-related research and formulation of more effective treatment strategies.

摘要

作为神经胶质瘤免疫微环境的主要组成部分之一,神经胶质瘤相关巨噬细胞(GAMs)越来越受到研究关注。GAMs 主要由固有小胶质细胞和外周衍生的单核巨噬细胞组成,其在多种活动中具有重要作用,如肿瘤细胞对化疗和放疗的抵抗以及促进神经胶质瘤发病机制。除了深入研究 GAM 极化外,对肿瘤微环境募集相关机制的研究也逐渐增多。抑制 GAMs 的来源可能会产生更好的治疗效果。在这里,我们总结了 GAMs 的起源和募集机制,以及 GAM 抑制的治疗意义,以促进未来与神经胶质瘤相关的研究和制定更有效的治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5f/10157099/7563817048ef/fimmu-14-1067641-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5f/10157099/c43d43cf8200/fimmu-14-1067641-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5f/10157099/81d4586b0beb/fimmu-14-1067641-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5f/10157099/7563817048ef/fimmu-14-1067641-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5f/10157099/c43d43cf8200/fimmu-14-1067641-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5f/10157099/81d4586b0beb/fimmu-14-1067641-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e5f/10157099/7563817048ef/fimmu-14-1067641-g003.jpg

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J Clin Invest. 2022 Jul 1;132(13). doi: 10.1172/JCI153563.
3
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Naunyn Schmiedebergs Arch Pharmacol. 2025 May;398(5):5437-5452. doi: 10.1007/s00210-024-03601-x. Epub 2024 Nov 19.
4
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Transl Psychiatry. 2024 Aug 23;14(1):338. doi: 10.1038/s41398-024-03019-2.
5
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