ArticleFrontiers in immunology2023
ChemR23 activation reprograms macrophages toward a less inflammatory phenotype and dampens carcinoma progression.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Cell-Surface Signatures and Targets of Modulated Vascular Smooth Muscle Cells in Atherosclerosis: From State Identification to Precision Intervention.Journal of cardiovascular development and disease · 2026Review
- Advances in Therapeutic Antibody Discovery and Development Targeting G Protein-Coupled Receptors.Pharmacology research & perspectives · 2026Review
- Chemerin and Asprosin as Promising Biomarkers of Metabolic Syndrome: A Scoping Review.Current obesity reports · 2025Article
- Monoclonal Antibody 5F1 Modulates Formyl Peptide Receptor 1 Conformation for Transmembrane Signaling.FASEB bioAdvances · 2025Article
- The Role of Chemerin in Neutrophil Activation and Diseases of the Lung.Biomedicines · 2025Review
- Immune inhibitory receptor agonist therapeutics.Frontiers in immunology · 2025Review
- The Involvement of Resolvins in Pathological Mechanisms of Periodontal Disease Associated with Type 2 Diabetes: A Narrative Review.International journal of molecular sciences · 2024Review
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- Nature of the Association between Rheumatoid Arthritis and Cervical Cancer and Its Potential Therapeutic Implications.Nutrients · 2024Review
- Stress in the metastatic journey - the role of cell communication and clustering in breast cancer progression and treatment resistance.Disease models & mechanisms · 2024Article
- The involvement of cyclin-dependent kinase 7 (CDK7) and 9 (CDK9) in coordinating transcription and cell cycle checkpoint regulation.Cell cycle (Georgetown, Tex.)Review
Corrections and comments
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Authors and funding
15 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Tumor Associated Macrophages (TAM) are a major component of the tumor environment and their accumulation often correlates with poor prognosis by contributing to local inflammation, inhibition of anti-tumor immune response and resistance to anticancer treatments. In this study, we thus investigated the anti-cancer therapeutic interest to target ChemR23, a receptor of the resolution of inflammation expressed by macrophages, using an agonist monoclonal antibody, αChemR23. Methods: Human GM-CSF, M-CSF and Tumor Associated Macrophage (TAM)-like macrophages were obtained by incubation of monocytes from healthy donors with GM-CSF, M-CSF or tumor cell supernatants (Breast cancer (BC) or malignant pleural mesothelioma (MPM) cells). The effects of αChemR23 on macrophages were studied at the transcriptomic, protein and functional level. Datasets from The Cancer Genome Atlas (TCGA) were used to study Results: We show that ChemR23 is expressed at higher levels in M-CSF and tumor cell supernatant differentiated macrophages (TAM-like) than in GM-CSF-differentiated macrophages. ChemR23 activation triggered by αChemR23 deeply modulates M-CSF and TAM-like macrophages including profile of cell surface markers, cytokine secretion, gene mRNA expression and immune functions. The expression of ChemR23 coding gene ( Conclusion: These results open an attractive opportunity to target TAM and the resolution of inflammation pathways through ChemR23 to circumvent TAM pro-tumoral effects.
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