ArticleJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research2012
Tumor-cell co-culture induced alternative activation of macrophages is modulated by interferons in vitro.
Article in Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
- GM-CSF downregulates type I IFN responses in glioblastoma-associated monocytes.Experimental & molecular medicine · 2026Article
- Review
- Type I interferon pathway activation in connective tissue disease associated interstitial lung disease.Frontiers in immunology · 2026Review
- PARP14 Contributes to the Development of the Tumor-Associated Macrophage Phenotype.International journal of molecular sciences · 2024Article
- Prevention of M2 polarization and temporal limitation of differentiation in monocytes by extracellular ATP.BMC immunology · 2023Article
- Tumor Cells Modulate Macrophage Phenotype in a Novel In Vitro Co-Culture Model of the NSCLC Tumor Microenvironment.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2022Article
- Phosphoinositide 3-kinase/Akt and its related signaling pathways in the regulation of tumor-associated macrophages polarization.Molecular and cellular biochemistry · 2022Review
- BQ-AurIPr: a redox-active anticancer Au(i) complex that induces immunogenic cell death.Chemical science · 2022Article
- CCL18 Expression Is Higher in a Glioblastoma Multiforme Tumor than in the Peritumoral Area and Causes the Migration of Tumor Cells Sensitized by Hypoxia.International journal of molecular sciences · 2022Article
- Glycyrrhizin prevents SARS-CoV-2 S1 and Orf3a induced high mobility group box 1 (HMGB1) release and inhibits viral replication.Cytokine · 2021Article
- From Toxicity to Selectivity: Coculture of the Fluorescent Tumor and Non-Tumor Lung Cells and High-Throughput Screening of Anticancer Compounds.Frontiers in pharmacology · 2021Article
- CCL18 in the Progression of Cancer.International journal of molecular sciences · 2020Review
- Plasmodium infection inhibits tumor angiogenesis through effects on tumor-associated macrophages in a murine implanted hepatoma model.Cell communication and signaling : CCS · 2020Article
- Mechanism of Xu Li's Experiential Prescription for the Treatment of EGFR-Positive NSCLC.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- Matrix stiffness and tumor-associated macrophages modulate epithelial to mesenchymal transition of human adenocarcinoma cells.Biofabrication · 2018Article
- Article
- Cytokine profiling of docetaxel-resistant castration-resistant prostate cancer.British journal of cancer · 2015Article
- Mitogen-Activated Protein Kinase Pathway: A Critical Regulator in Tumor-associated Macrophage Polarization.Journal of microscopy and ultrastructureReview
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor-associated macrophages infiltrate tumors and facilitate tumor growth. Here, we analyzed M1 and M2 marker expression in the course of co-culture-driven macrophage differentiation and investigated the influence of interferons (IFNs) on this differentiation. To generate monocyte-derived macrophages (MDMs) 1×10⁶ monocytes of healthy volunteers were cultivated either with 25×10³ adherent A549/mL or in medium containing 50% A549 conditioned medium (CM) for 72 h in the presence or absence of IFN-α, β or γ, respectively. Supernatants were tested for CCL18 (M2 marker) and CXCL10 (M1 marker) by enzyme-linked immunosorbent assay. CCL18 and CXCL10 release by MDM is increased by the presence of A549 cells, but also when cultured in A549 CM. On stimulation with IFN-γ, we observe an increased release of the M1 marker CXCL10 and a decreased release of CCL18. Type I IFNs also increases CXCL10 release. Thus, A549 releases a soluble factor which enhances CCL18 production and M2 polarization, indicating that a localized specific cytokine milieu, as found in the environment of a tumor or in fibrotic lung tissue, favors alternative activation of macrophages. In the presence of IFN-γ, M2 differentiation is attenuated as shown by the decrease of the M2 chemokine CCL18 and by the increase of the M1 chemokine CXCL10. However, CXCL10 levels were also increased by the co-culture, which indicates a simultaneous classical activation (M1) or the formation of a M1/M2 hybrid.
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Registered trials
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.