Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (818 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Glycoproteins found in a subfraction of normal mammalian plasma and urine. They stimulate the proliferation of bone marrow cells in agar cultures and the formation of colonies of granulocytes and/or macrophages. The factors include interleukin-3; (IL-3); granulocyte colony-stimulating factor; (g-csf); macrophage colony-stimulating factor; (m-csf); and granulocyte-macrophage colony-stimulating factor; (gm-csf).
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Colony Stimulating Factors; Colony Stimulating Factor; Colony-Stimulating Factor; MGI-1 Protein; MGI 1 Protein; MGI-1; Myeloid Cell-Growth Inducer; Cell-Growth Inducer, Myeloid.
Where it fits in the MeSH classification
- Broader topics
- Glycoproteins; Hematopoietic Cell Growth Factors
- Narrower topics
- Erythropoietin; Granulocyte Colony-Stimulating Factor; Granulocyte-Macrophage Colony-Stimulating Factor; Interleukin-3; Macrophage Colony-Stimulating Factor; Thrombopoietin
- See also
- Receptors, Colony-Stimulating Factor
Related concepts
Research landscape
PubMed indexes 70,890 records tagged with the MeSH heading “Colony-Stimulating Factors” (counts retrieved 2026-10-31). 6,520 of them (9.2%) were published from 2020 onward, and the busiest period so far is through 1999 with 29,068 records.
Reviews account for 8,402 records (11.9%) and meta-analyses for 421. Randomized controlled trials number 3,223 (4.5%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 29,068 |
| 2000-2009 | 20,168 |
| 2010-2019 | 15,134 |
| 2020 onward | 6,520 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 8,402 | 11.9% |
| Meta-analyses | 421 | 0.6% |
| Randomized controlled trials | 3,223 | 4.5% |
Method: PubMed query "Colony-Stimulating Factors"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Macrophages promote pre-metastatic niche formation of breast cancer through aryl hydrocarbon receptor activity | 2024 | Research article Design not recorded in structured metadata | 46 | cc by PMID 39690159 · DOI · PMC11652640 |
| Synovial macrophage diversity and activation of M-CSF signaling in post-traumatic osteoarthritis | 2025 | Research article Design not recorded in structured metadata | 35 | cc by PMID 39969512 · DOI · PMC11839164 |
| The anti-GD2 monoclonal antibody naxitamab plus GM-CSF for relapsed or refractory high-risk neuroblastoma: a phase 2 clinical trial | 2025 | Research article Design not recorded in structured metadata | 26 | cc by PMID 39952926 · DOI · PMC11828896 |
| Microglial colonization of the developing mouse brain is controlled by both microglial and neural CSF-1 | 2026 | Research article Design not recorded in structured metadata | 6 | cc by PMID 41249504 · DOI · PMC12759073 |
Macrophages promote pre-metastatic niche formation of breast cancer through aryl hydrocarbon receptor activity [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Macrophages that acquire an immunosuppressive phenotype play a crucial role in establishing the pre-metastatic niche (PMN), which is essential for facilitating breast cancer metastasis to distant organs.
- Closing excerpt
- These findings reveal that the crosstalk of breast cancer cells, lung macrophages, and Treg cells via the GM-CSF-STAT5-AHR-PD-L1 cascade modulates the lung pre-metastatic niche during breast cancer progression.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (200 words)
Macrophages that acquire an immunosuppressive phenotype play a crucial role in establishing the pre-metastatic niche (PMN), which is essential for facilitating breast cancer metastasis to distant organs. Our study showed that increased activity of the aryl hydrocarbon receptor (AHR) in lung macrophages plays a crucial role in establishing the immunosuppressive PMN in breast cancer. Specifically, AHR activation led to high expression of PD-L1 on macrophages by directly binding to the promoter of Pdl1. This upregulation of PD-L1 promoted the differentiation of regulatory T cells (Tregs) within the PMN, further enhancing immunosuppressive conditions. Mice with Ahr conditional deletion in macrophages had reduced lung metastasis of breast cancer. The elevated AHR levels in PMN macrophages were induced by GM-CSF, which was secreted by breast cancer cells. Mechanistically, the activated STAT5 signaling pathway induced by GM-CSF prevented AHR from being ubiquitinated, thereby sustaining its activity in macrophages. In breast cancer patients, the expression of AHR and PD-L1 was correlated with increased Treg cell infiltration, and higher levels of AHR were associated with a poor prognosis. These findings reveal that the crosstalk of breast cancer cells, lung macrophages, and Treg cells via the GM-CSF-STAT5-AHR-PD-L1 cascade modulates the lung pre-metastatic niche during breast cancer progression.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39690159 · DOI · PMC11652640
Synovial macrophage diversity and activation of M-CSF signaling in post-traumatic osteoarthritis [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Synovium is home to immune and stromal cell types that orchestrate inflammation following a joint injury; in particular, macrophages are central protagonists in this process.
- Closing excerpt
- Nuanced characterization of the distinct functions, origins, and disease kinetics of macrophage subtypes in PTOA will be critical for targeting these highly versatile cells for therapeutic purposes.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (236 words)
Synovium is home to immune and stromal cell types that orchestrate inflammation following a joint injury; in particular, macrophages are central protagonists in this process. We sought to define the cellular and temporal dynamics of the synovial immune niche in a mouse model of post-traumatic osteoarthritis (PTOA), and to identify stromal-immune crosstalk mechanisms that coordinate macrophage function and phenotype. We induced PTOA in mice using a non-invasive tibial compression model of anterior cruciate ligament rupture (ACLR). Single-cell RNA-sequencing and flow cytometry were used to assess immune cell populations in healthy (Sham) and injured (7 and 28 days post-ACLR) synovium. Characterization of synovial macrophage polarization states was performed, alongside computational modeling of macrophage differentiation, as well as implicated transcriptional regulators and stromal-immune communication axes. Immune cell types are broadly represented in healthy synovium, but experience drastic expansion and speciation in PTOA, most notably in the macrophage portion. We identified several polarization states of macrophages in synovium following joint injury, underpinned by distinct transcriptomic signatures, and regulated in part by stromal-derived macrophage colony-stimulating factor signaling. The transcription factors Pu.1, Cebpα, Cebpβ, and Jun were predicted to control differentiation of systemically derived monocytes into pro-inflammatory synovial macrophages. In summary, we defined different synovial macrophage subpopulations present in healthy and injured mouse synovium. Nuanced characterization of the distinct functions, origins, and disease kinetics of macrophage subtypes in PTOA will be critical for targeting these highly versatile cells for therapeutic purposes.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39969512 · DOI · PMC11839164
The anti-GD2 monoclonal antibody naxitamab plus GM-CSF for relapsed or refractory high-risk neuroblastoma: a phase 2 clinical trial [3]
Abstract reading summary — source excerpts
- Opening excerpt
- In this single-arm, non-randomized, phase 2 trial (NCT03363373), 74 patients with relapsed/refractory high-risk neuroblastoma and residual disease in bone/bone marrow (BM) received naxitamab on Days 1, 3, and 5 (3 mg/kg/day) with granulocyte-macrophage colony-stimulating factor (Days -4 to 5) every 4 weeks, until complete response (CR) or partial response (PR) followed by 5 additional cycles every 4 weeks.
- Closing excerpt
- Overall, naxitamab demonstrated clinically meaningful efficacy with manageable safety in patients with residual neuroblastoma in bone/BM.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (203 words)
In this single-arm, non-randomized, phase 2 trial (NCT03363373), 74 patients with relapsed/refractory high-risk neuroblastoma and residual disease in bone/bone marrow (BM) received naxitamab on Days 1, 3, and 5 (3 mg/kg/day) with granulocyte-macrophage colony-stimulating factor (Days -4 to 5) every 4 weeks, until complete response (CR) or partial response (PR) followed by 5 additional cycles every 4 weeks. Primary endpoint in the prespecified interim analysis was overall response (2017 International Neuroblastoma Response Criteria). Among 26 responders (CR + PR) in the efficacy population (N = 52), 58% had refractory disease, and 42% had relapsed disease. Overall response rate (ORR) was 50% (95% CI: 36-64%), and CR and PR were observed in 38% and 12%, respectively. With the 95% CI lower limit for ORR exceeding 20%, the primary endpoint of overall response was met. Patients with evaluable bone disease had a 58% (29/50) bone compartment response (CR, 40%; PR, 18%). BM compartment response was 74% (17/23; CR, 74%). One-year overall survival and progression-free survival (secondary endpoints) were 93% (95% CI: 80-98%) and 35% (95% CI: 16-54%), respectively. Naxitamab-related Grade 3 adverse events included hypotension (58%) and pain (54%). Overall, naxitamab demonstrated clinically meaningful efficacy with manageable safety in patients with residual neuroblastoma in bone/BM.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39952926 · DOI · PMC11828896
Microglial colonization of the developing mouse brain is controlled by both microglial and neural CSF-1 [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Microglia are brain-resident macrophages critical for cerebral development, function, and homeostasis.
- Closing excerpt
- Our study reveals that microglia rely on distinct, local, and cell-type-specific sources of CSF-1 for their developmental distribution, which has major implications for understanding how microglia colonize the brain in health and disease.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (179 words)
Microglia are brain-resident macrophages critical for cerebral development, function, and homeostasis. During development, yolk sac-derived microglial progenitor cells colonize and populate the brain following a well-defined spatiotemporal pattern. However, the mechanisms controlling microglial colonization and proliferation remain largely unknown. Here, we describe two broad waves of microglial proliferation in the developing mouse forebrain. Microglia accumulate in transient hotspots, in a proliferative axon tract-associated microglia (ATM)-like state. Prenatal and early postnatal patterns of microglial colonization do not rely on neuronal activity. Instead, using conditional inactivation of the microglial regulator colony-stimulating factor 1 (Csf1) gene, we reveal that the distribution and proliferation of embryonic cortical microglia critically rely on neural CSF-1, mainly produced by cortical progenitor cells but also by post-mitotic neurons, with the action of CSF-1 being local, dose-dependent, and transient. In addition, intrinsic CSF-1 expressed by ATM microglia contributes to their sustained proliferation in developmental hotspots. Our study reveals that microglia rely on distinct, local, and cell-type-specific sources of CSF-1 for their developmental distribution, which has major implications for understanding how microglia colonize the brain in health and disease.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41249504 · DOI · PMC12759073
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article The effect of HIF on metabolism and immunity [5]
- Research article Mortality and target haemoglobin concentrations in anaemic patients with chronic kidney disease treated with erythropoietin: a meta-analysis [6]
- Research article GM-CSF: A Double-Edged Sword in Cancer Immunotherapy [7]
- Research article Colony-stimulating factors for chemotherapy-induced febrile neutropenia: a meta-analysis of randomized controlled trials [8]
- Research article Granulocyte colony-stimulating factors for febrile neutropenia prophylaxis following chemotherapy: systematic review and meta-analysis [9]
- Research article Granulocyte-colony stimulating factor (G-CSF) and granulocyte-macrophage colony stimulating factor (GM-CSF) for sepsis: a meta-analysis [10]
References
- Jiang X, Wang J, Lin L, Du L, Ding Y, Zheng F, et al.. Macrophages promote pre-metastatic niche formation of breast cancer through aryl hydrocarbon receptor activity. . 2024. PMID 39690159 · DOI · PMC11652640
- Knights AJ, Farrell EC, Ellis OM, Song MJ, Appleton CT, Maerz T. Synovial macrophage diversity and activation of M-CSF signaling in post-traumatic osteoarthritis. . 2025. PMID 39969512 · DOI · PMC11839164
- Mora J, Chan GCF, Morgenstern DA, Amoroso L, Nysom K, Faber J, et al.. The anti-GD2 monoclonal antibody naxitamab plus GM-CSF for relapsed or refractory high-risk neuroblastoma: a phase 2 clinical trial. . 2025. PMID 39952926 · DOI · PMC11828896
- Bridlance C, Viguier S, Olivié N, Dupont E, Thobois D, Mathieu B, et al.. Microglial colonization of the developing mouse brain is controlled by both microglial and neural CSF-1. . 2026. PMID 41249504 · DOI · PMC12759073
- Taylor CT, Scholz CC. The effect of HIF on metabolism and immunity. Nat Rev Nephrol. 2022. PMID 35726016 · DOI · PMC9208707
- Phrommintikul A, Haas SJ, Elsik M, Krum H. Mortality and target haemoglobin concentrations in anaemic patients with chronic kidney disease treated with erythropoietin: a meta-analysis. Lancet. 2007. PMID 17276778 · DOI
- Kumar A, Taghi Khani A, Sanchez Ortiz A, Swaminathan S. GM-CSF: A Double-Edged Sword in Cancer Immunotherapy. Front Immunol. 2022. PMID 35865534 · DOI · PMC9294178
- Clark OA, Lyman GH, Castro AA, Clark LG, Djulbegovic B. Colony-stimulating factors for chemotherapy-induced febrile neutropenia: a meta-analysis of randomized controlled trials. J Clin Oncol. 2005. PMID 15961767 · DOI
- Cooper KL, Madan J, Whyte S, Stevenson MD, Akehurst RL. Granulocyte colony-stimulating factors for febrile neutropenia prophylaxis following chemotherapy: systematic review and meta-analysis. BMC Cancer. 2011. PMID 21943360 · DOI · PMC3203098
- Bo L, Wang F, Zhu J, Li J, Deng X. Granulocyte-colony stimulating factor (G-CSF) and granulocyte-macrophage colony stimulating factor (GM-CSF) for sepsis: a meta-analysis. Crit Care. 2011. PMID 21310070 · DOI · PMC3221991
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.