ArticleOncoimmunology2016
Murine mesothelioma induces locally-proliferating IL-10(+)TNF-α(+)CD206(-)CX3CR1(+) M3 macrophages that can be selectively depleted by chemotherapy or immunotherapy.
Article in Oncoimmunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 68 citations in OpenAlex.
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- Harnessing amino acid pathways to influence myeloid cell function in tumor immunity.Molecular medicine (Cambridge, Mass.) · 2025Review
- Interleukin-27-polarized HIV-resistant M2 macrophages are a novel subtype of macrophages that express distinct antiviral gene profiles in individual cells: implication for the antiviral effect via different mechanisms in the individual cell-dependent manner.Frontiers in immunology · 2025Article
- Clinical Perspectives and Novel Preclinical Models of Malignant Pleural Mesothelioma: A Critical Review.ACS pharmacology & translational science · 2024Review
- Antibody targeting of anaerobic bacteria warms cold tumors and improves the abscopal effect of radiotherapy.Journal of translational medicine · 2024Article
- Macrophages, Metabolism, Mitochondria, Circadian Rhythmicity and the Pathogen: The Multidimensional Nature of Tuberculosis.Results and problems in cell differentiation · 2024Review
- Blockage of CacyBP inhibits macrophage recruitment and improves anti-PD-1 therapy in hepatocellular carcinoma.Journal of experimental & clinical cancer research : CR · 2023Article
- Cholinergic Polarization of Human Macrophages.International journal of molecular sciences · 2023Review
- Adipose tissue macrophages: implications for obesity-associated cancer.Military Medical Research · 2023Review
- Macrophage/microglia polarization for the treatment of diabetic retinopathy.Frontiers in endocrinology · 2023Review
- Chaperone-assisted E3 ligase CHIP: A double agent in cancer.Genes & diseases · 2022Review
- Immunotherapy approaches for malignant pleural mesothelioma.Nature reviews. Clinical oncology · 2022Review
- IFN-γ enhances the antitumor activity of attenuatedFrontiers in bioengineering and biotechnology · 2022Article
- The STING agonist, DMXAA, reduces tumor vessels and enhances mesothelioma tumor antigen presentation yet blunts cytotoxic T cell function in a murine model.Frontiers in immunology · 2022Article
- Aging Leads to Increased Monocytes and Macrophages With Altered CSF-1 Receptor Expression and Earlier Tumor-Associated Macrophage Expansion in Murine Mesothelioma.Frontiers in aging · 2022Article
- A vicious circle in breast cancer: The interplay between inflammation, reactive oxygen species, and microRNAs.Frontiers in oncology · 2022Review
- Matter of TIME: the tumor-immune microenvironment of mesothelioma and implications for checkpoint blockade efficacy.Journal for immunotherapy of cancer · 2021Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We used a murine model to monitor changes to myeloid cell subsets, i.e., myeloid-derived suppressor cells (MDSCs), M1 macrophages that secrete pro-inflammatory cytokines and express CD40 and CD80 and suppressive M2 macrophages that secrete anti-inflammatory cytokines and express CD206 and CX3CR1, during mesothelioma progression and during chemotherapy or immunotherapy-induced tumor regression. In vitro studies showed that mesothelioma-conditioned media generated CD206(-)CX3CR1(+)MCP-1(+)TGF-β(+) macrophages that induced T cell proliferation but prevented T cell IFNγ production. In vivo studies showed that co-inoculation of macrophages with mesothelioma cells led to faster tumor growth, and depleting macrophages using anti-F4/80 antibody induced tumor regression. Flow cytometry revealed increasing levels of different suppressive myeloid cells in lymphoid organs: MDSCs dominated bone marrow (BM) and spleens, M2 macrophages dominated tumor-draining lymph nodes (DLN) and a mixed IL-10(+)TNF-α(+)CD206(-)CX3CR1(+) M1/M2 (M3) macrophage subset dominated the mesothelioma microenvironment. Ki67 staining and cell cycle analysis showed that tumor-associated M1 and M3, but not M2, macrophages were proliferating in situ, with M1 cells arrested in the G1 phase while M3 cells progressed to mitosis. Immunohistochemistry showed that M1 and M3 cells were co-located supporting the hypothesis that M1 cells transition to M3 cells during proliferation. Gemcitabine reduced tumor-associated M3 and MDSCs, but not M2 macrophages, the latter likely contributing to the tumor outgrowth seen following treatment cessation. In contrast, IL-2/agonist anti-CD40 antibody therapy reduced M3 cells and polarized macrophages into M1 cells coinciding with tumor regression. These data show that myeloid cells, particularly M3 cells, represent a therapeutic target for the generation of antitumor immunity.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.