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Published in: Journal of Cancer Research and Clinical Oncology 5/2024

Open Access 01-05-2024 | Review

The role of tumor-associated macrophages in tumor immune evasion

Authors: Ruizhe Huang, Ting Kang, Siyu Chen

Published in: Journal of Cancer Research and Clinical Oncology | Issue 5/2024

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Abstract

Background

Tumor growth is closely linked to the activities of various cells in the tumor microenvironment (TME), particularly immune cells. During tumor progression, circulating monocytes and macrophages are recruited, altering the TME and accelerating growth. These macrophages adjust their functions in response to signals from tumor and stromal cells. Tumor-associated macrophages (TAMs), similar to M2 macrophages, are key regulators in the TME.

Methods

We review the origins, characteristics, and functions of TAMs within the TME. This analysis includes the mechanisms through which TAMs facilitate immune evasion and promote tumor metastasis. Additionally, we explore potential therapeutic strategies that target TAMs.

Results

TAMs are instrumental in mediating tumor immune evasion and malignant behaviors. They release cytokines that inhibit effector immune cells and attract additional immunosuppressive cells to the TME. TAMs primarily target effector T cells, inducing exhaustion directly, influencing activity indirectly through cellular interactions, or suppressing through immune checkpoints. Additionally, TAMs are directly involved in tumor proliferation, angiogenesis, invasion, and metastasis.

Summary

Developing innovative tumor-targeted therapies and immunotherapeutic strategies is currently a promising focus in oncology. Given the pivotal role of TAMs in immune evasion, several therapeutic approaches have been devised to target them. These include leveraging epigenetics, metabolic reprogramming, and cellular engineering to repolarize TAMs, inhibiting their recruitment and activity, and using TAMs as drug delivery vehicles. Although some of these strategies remain distant from clinical application, we believe that future therapies targeting TAMs will offer significant benefits to cancer patients.
Literature
go back to reference Jayaraman P, Parikh F, Lopez-Rivera E, Hailemichael Y, Clark A, Ma G, Sikora AG (2012) Tumor-expressed inducible nitric oxide synthase controls induction of functional myeloid-derived suppressor cells through modulation of vascular endothelial growth factor release. J Immunol 188(11):5365–5376. https://doi.org/10.4049/jimmunol.1103553CrossRefPubMed Jayaraman P, Parikh F, Lopez-Rivera E, Hailemichael Y, Clark A, Ma G, Sikora AG (2012) Tumor-expressed inducible nitric oxide synthase controls induction of functional myeloid-derived suppressor cells through modulation of vascular endothelial growth factor release. J Immunol 188(11):5365–5376. https://​doi.​org/​10.​4049/​jimmunol.​1103553CrossRefPubMed
go back to reference Koru-Sengul T, Santander AM, Miao F, Sanchez LG, Jorda M, Gluck S, Torroella-Kouri M (2016) Breast cancers from black women exhibit higher numbers of immunosuppressive macrophages with proliferative activity and of crown-like structures associated with lower survival compared to non-black Latinas and Caucasians. Breast Cancer Res Treat 158(1):113–126. https://doi.org/10.1007/s10549-016-3847-3CrossRefPubMedPubMedCentral Koru-Sengul T, Santander AM, Miao F, Sanchez LG, Jorda M, Gluck S, Torroella-Kouri M (2016) Breast cancers from black women exhibit higher numbers of immunosuppressive macrophages with proliferative activity and of crown-like structures associated with lower survival compared to non-black Latinas and Caucasians. Breast Cancer Res Treat 158(1):113–126. https://​doi.​org/​10.​1007/​s10549-016-3847-3CrossRefPubMedPubMedCentral
Metadata
Title
The role of tumor-associated macrophages in tumor immune evasion
Authors
Ruizhe Huang
Ting Kang
Siyu Chen
Publication date
01-05-2024
Publisher
Springer Berlin Heidelberg
Published in
Journal of Cancer Research and Clinical Oncology / Issue 5/2024
Print ISSN: 0171-5216
Electronic ISSN: 1432-1335
DOI
https://doi.org/10.1007/s00432-024-05777-4

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