ArticleCancer immunology, immunotherapy : CII2010
Type I interferons inhibit the generation of tumor-associated macrophages.
Article in Cancer immunology, immunotherapy : CII, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
19 citing papers in PubMed, 54 citations in OpenAlex.
- Context-dependent impact of type I interferon signaling in cancer.Molecular cancer · 2025Review
- The role of type I interferon signaling in myeloid anti-tumor immunity.Frontiers in immunology · 2025Review
- Review
- Hypoxic glioblastoma-cell-derived extracellular vesicles impair cGAS-STING activity in macrophages.Cell communication and signaling : CCS · 2024Article
- Metabolic mediators: microbial-derived metabolites as key regulators of anti-tumor immunity, immunotherapy, and chemotherapy.Frontiers in immunology · 2024Review
- Inhibitory receptors of plasmacytoid dendritic cells as possible targets for checkpoint blockade in cancer.Frontiers in immunology · 2024Review
- Reprogramming of tumor-associated macrophages via NEDD4-mediated CSF1R degradation by targeting USP18.Cell reports · 2023Article
- SPOP Mutations Target STING1 Signaling in Prostate Cancer and Create Therapeutic Vulnerabilities to PARP Inhibitor-Induced Growth Suppression.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
- cGAS-STING Pathway as the Target of Immunotherapy for Lung Cancer.Current cancer drug targets · 2023Review
- Systemic vaccination induces CD8Cell · 2022Article
- The microbiome-derived metabolite TMAO drives immune activation and boosts responses to immune checkpoint blockade in pancreatic cancer.Science immunology · 2022Article
- Modulation of Type I Interferon Responses to Influence Tumor-Immune Cross Talk in PDAC.Frontiers in cell and developmental biology · 2022Review
- Opposing Roles of Type I Interferons in Cancer Immunity.Annual review of pathology · 2021Review
- The Function of cGAS-STING Pathway in Treatment of Pancreatic Cancer.Frontiers in immunology · 2021Review
- Interactions among myeloid regulatory cells in cancer.Cancer immunology, immunotherapy : CII · 2019Review
- HLA class II expression on tumor cells and low numbers of tumor-associated macrophages predict clinical outcome in oropharyngeal cancer.Head & neck · 2019Article
- Concomitant type I IFN and M-CSF signaling reprograms monocyte differentiation and drives pro-tumoral arginase production.EBioMedicine · 2019Article
- Pro-Tumoral Inflammatory Myeloid Cells as Emerging Therapeutic Targets.International journal of molecular sciences · 2016Review
- Emerging role of tumor-associated macrophages as therapeutic targets in patients with metastatic renal cell carcinoma.Cancer immunology, immunotherapy : CII · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Tumor-associated macrophages (TAM) are very abundant in tumors and are thought to play a major role in promoting tumor growth. The generation of TAM is positively regulated by several cytokines, including colony stimulating factor-1 (CSF-1) and monocyte chemoattractant protein-1 (CCL2). However, endogenous factors that suppress the generation of TAM within tumors have not been previously identified. An earlier study showed that endogenously produced type I interferons (IFN) suppressed tumor growth via their effects on hematopoietic cells rather than through direct effects on tumor cells. Therefore, we used mouse tumor models to investigate the effects of endogenously produced type I IFNs on the generation of TAM. We found using immunohistochemistry and flow cytometry that TAM density was significantly increased in tumors of mice lacking the type I IFN receptor (IFN-alpha/betaR(-/-) mice) compared to wild type mice. Moreover, the increase in TAM density was associated with a significant increase in tumor growth rate and angiogenesis. The phenotype of TAM was similar in IFN-alpha/betaR(-/-) mice and wild type mice and tumors in both mice produced similar amounts of CSF-1 and CCL2. However, in vitro assays indicated that low concentrations of type I IFNs significantly inhibited the generation of bone marrow macrophages in response to CSF-1. These findings indicate that endogenously produced type I IFNs suppress the generation of TAM, which may in turn account for inhibition of tumor growth and angiogenesis.
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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.