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肿瘤相关巨噬细胞亚群：塑造极化和靶向。

Tumor-Associated Macrophage Subsets: Shaping Polarization and Targeting.

机构信息

Division of Cancer Medicine, Department of Cancer Immunology, Oslo University Hospital, University of Oslo, Ullernchausseen 70, 0379 Oslo, Norway.

Department of Pharmacy, Faculty of Mathematics and Natural Sciences, University of Oslo, Blindern, P.O. Box 1068, 0316 Oslo, Norway.

出版信息

Int J Mol Sci. 2023 Apr 19;24(8):7493. doi: 10.3390/ijms24087493.

DOI:10.3390/ijms24087493
PMID:37108657
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10138703/
Abstract

The tumor microenvironment (TME) is a critical regulator of tumor growth, progression, and metastasis. Among the innate immune cells recruited to the tumor site, macrophages are the most abundant cell population and are present at all stages of tumor progression. They undergo M1/M2 polarization in response to signals derived from TME. M1 macrophages suppress tumor growth, while their M2 counterparts exert pro-tumoral effects by promoting tumor growth, angiogenesis, metastasis, and resistance to current therapies. Several subsets of the M2 phenotype have been observed, often denoted as M2a, M2b, M2c, and M2d. These are induced by different stimuli and differ in phenotypes as well as functions. In this review, we discuss the key features of each M2 subset, their implications in cancers, and highlight the strategies that are being developed to harness TAMs for cancer treatment.

摘要

肿瘤微环境（TME）是肿瘤生长、进展和转移的关键调节者。在募集到肿瘤部位的固有免疫细胞中，巨噬细胞是最丰富的细胞群体，存在于肿瘤进展的所有阶段。它们根据源自 TME 的信号发生 M1/M2 极化。M1 巨噬细胞抑制肿瘤生长，而它们的 M2 对应物通过促进肿瘤生长、血管生成、转移和对现有治疗方法的耐药性来发挥促肿瘤作用。已经观察到 M2 表型的几个亚群，通常表示为 M2a、M2b、M2c 和 M2d。这些是由不同的刺激物诱导的，在表型和功能上有所不同。在这篇综述中，我们讨论了每个 M2 亚群的关键特征、它们在癌症中的意义，并强调了正在开发的利用 TAMs 进行癌症治疗的策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe60/10138703/23997cb16e9c/ijms-24-07493-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe60/10138703/5dc7bb981c5c/ijms-24-07493-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe60/10138703/4118829f1004/ijms-24-07493-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe60/10138703/0a8d9fd29396/ijms-24-07493-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe60/10138703/ec45803e6c66/ijms-24-07493-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe60/10138703/169b86a99b6e/ijms-24-07493-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe60/10138703/23997cb16e9c/ijms-24-07493-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe60/10138703/5dc7bb981c5c/ijms-24-07493-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe60/10138703/4118829f1004/ijms-24-07493-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe60/10138703/0a8d9fd29396/ijms-24-07493-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe60/10138703/ec45803e6c66/ijms-24-07493-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe60/10138703/169b86a99b6e/ijms-24-07493-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe60/10138703/23997cb16e9c/ijms-24-07493-g006.jpg

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[3]
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[4]
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[5]
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[6]
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[7]
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[8]
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[9]
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[10]
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本文引用的文献

[1]
The New Frontier of Immunotherapy: Chimeric Antigen Receptor T (CAR-T) Cell and Macrophage (CAR-M) Therapy against Breast Cancer.

Cancers (Basel). 2023-3-4

[2]
The IL-10 receptor inhibits cell extrinsic signals necessary for STAT1-dependent macrophage accumulation during colitis.

Mucosal Immunol. 2023-6

[3]
Fibronectin 1 derived from tumor-associated macrophages and fibroblasts promotes metastasis through the JUN pathway in hepatocellular carcinoma.

Int Immunopharmacol. 2022-12

[4]
Crosstalk between Tumor-Associated Macrophages and MicroRNAs: A Key Role in Tumor Microenvironment.

Int J Mol Sci. 2022-10-31

[5]
Expression of O-glycosylated oncofetal fibronectin in alternatively activated human macrophages.

Immunol Res. 2023-2

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Sci Transl Med. 2022-8-3

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J Immunother Cancer. 2022-8

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Cells. 2022-6-25

[9]
The Overexpression of Fibronectin 1 Promotes Cancer Progression and Associated with M2 Macrophages Polarization in Head and Neck Squamous Cell Carcinoma Patients.

Int J Gen Med. 2022-5-17

[10]
Structural Requirements for the Binding of a Peptide to Prohibitins on the Cell Surface of Monocytes/Macrophages.

Int J Mol Sci. 2022-4-13

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