ArticleEBioMedicine2016
Targeting myeloid-derived suppressor cells with colony stimulating factor-1 receptor blockade can reverse immune resistance to immunotherapy in indoleamine 2,3-dioxygenase-expressing tumors.
Article in EBioMedicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 2 of them syntheses that pooled it.
What it found
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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
102 citing papers in PubMed, 2 syntheses or guidelines pooled it, 145 citations in OpenAlex.
- Targeting PI3K-gamma in myeloid driven tumour immune suppression: a systematic review and meta-analysis of the preclinical literature.Cancer immunology, immunotherapy : CII · 2024Pooled it
- Cutting edges and therapeutic opportunities on tumor-associated macrophages in lung cancer.Frontiers in immunology · 2022Pooled it
- Tryptophan metabolism in tumor microenvironment and therapeutic implications.Journal of advanced research · 2026Review
- Targeting GPR34 in damage-associated macrophages enhances anti-tumor immunity and the efficacy of Surufatinib in pancreatic cancer.Signal transduction and targeted therapy · 2026Article
- Macrophage polarization, inflammatory monocytes, and impaired MDSCs are associated with murine and human immune aplastic anemia.Journal of leukocyte biology · 2025Article
- Myeloid-Derived Suppressor Cells in Cancer: Mechanistic Insights and Targeted Therapeutic Innovations.MedComm · 2025Review
- Potential Mechanisms for Immunotherapy Resistance in Adult Soft-Tissue Sarcoma.Targeted oncology · 2025Review
- The immunosuppressive role of MDSCs in HCC: mechanisms and therapeutic opportunities.Cell communication and signaling : CCS · 2025Review
- Emerging Role of MDSCS as Novel Biomarkers and Therapeutic Targets for Cancer Immunotherapy.ImmunoTargets and therapy · 2025Review
- Cellular mechanisms of combining innate immunity activation with PD-1/PD-L1 blockade in treatment of colorectal cancer.Molecular cancer · 2024Review
- Insights into CSF-1R Expression in the Tumor Microenvironment.Biomedicines · 2024Review
- Role of indoleamine 2, 3-dioxygenase 1 in immunosuppression of breast cancer.Cancer pathogenesis and therapy · 2024Review
- Article
- Myeloid‑derived suppressor cells: Key immunosuppressive regulators and therapeutic targets in colorectal cancer (Review).International journal of oncology · 2024Review
- Locoregional therapies combined with immune checkpoint inhibitors for liver metastases.Cancer cell international · 2024Review
- Tumor battlefield within inflamed, excluded or desert immune phenotypes: the mechanisms and strategies.Experimental hematology & oncology · 2024Review
- Glioma-derived M-CSF and IL-34 license M-MDSCs to suppress CD8bioRxiv : the preprint server for biology · 2024Article
- Defining mesenchymal stem/stromal cell-induced myeloid-derived suppressor cells using single-cell transcriptomics.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Targeting inflammation as cancer therapy.Journal of hematology & oncology · 2024Review
- Immune modulation in malignant pleural effusion: from microenvironment to therapeutic implications.Cancer cell international · 2024Review
42 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Tumor indoleamine 2,3-dioxygenase (IDO) promotes immunosuppression by direct action on effector T cells and Tregs and through recruitment, expansion and activation of myeloid-derived suppressor cells (MDSCs). Targeting of MDSCs is clinically being explored as a therapeutic strategy, though optimal targeting strategies and biomarkers predictive of response are presently unknown. Maturation and tumor recruitment of MDSCs are dependent on signaling through the receptor tyrosine kinase CSF-1R on myeloid cells. Here, we show that MDSCs are the critical cell population in IDO-expressing B16 tumors in mediating accelerated tumor outgrowth and resistance to immunotherapy. Using a clinically relevant drug, we show that inhibition of CSF-1R signaling can functionally block tumor-infiltrating MDSCs and enhance anti-tumor T cell responses. Furthermore, inhibition of CSF-1R sensitizes IDO-expressing tumors to immunotherapy with T cell checkpoint blockade, and combination of CSF-1R blockade with IDO inhibitors potently elicits tumor regression. These findings provide evidence for a critical and functional role for MDSCs on the in vivo outcome of IDO-expressing tumors.
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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.