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 (730 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
A multilineage cell growth factor secreted by lymphocytes; epithelial cells; and astrocytes which stimulates clonal proliferation and differentiation of various types of blood and tissue cells.
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: Interleukin 3; Erythrocyte Burst-Promoting Factor; Erythrocyte Burst Promoting Factor; Colony-Stimulating Factor 2 Alpha; Colony-Stimulating Factor, Mast-Cell; Colony Stimulating Factor, Mast Cell; Mast-Cell Colony-Stimulating Factor; Colony-Stimulating Factor, Multipotential.
Where it fits in the MeSH classification
- Broader topics
- Colony-Stimulating Factors; Interleukins
- See also
- Receptors, Interleukin-3
Related concepts
- Lymphocytes
- Epithelial Cells
- Astrocytes
Research landscape
PubMed indexes 6,520 records tagged with the MeSH heading “Interleukin-3” (counts retrieved 2026-10-31). 178 of them (2.7%) were published from 2020 onward, and the busiest period so far is through 1999 with 4,429 records.
Reviews account for 402 records (6.2%) and meta-analyses for 4. Randomized controlled trials number 30 (0.5%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 4,429 |
| 2000-2009 | 1,382 |
| 2010-2019 | 531 |
| 2020 onward | 178 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 402 | 6.2% |
| Meta-analyses | 4 | 0.1% |
| Randomized controlled trials | 30 | 0.5% |
Method: PubMed query "Interleukin-3"[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 |
|---|---|---|---|---|
| Activated Stat5 trafficking Via Endothelial Cell-derived Extracellular Vesicles Controls IL-3 Pro-angiogenic Paracrine Action | 2016 | Research article Design not recorded in structured metadata | 71 | cc by PMID 27157262 · DOI · PMC4860593 |
| Innate Immune Modulation by GM-CSF and IL-3 in Health and Disease | 2019 | Review article Design not recorded in structured metadata | 55 | cc by PMID 30769926 · DOI · PMC6412223 |
| Interleukin-3 is a predictive marker for severity and outcome during SARS-CoV-2 infections | 2021 | Research article Design not recorded in structured metadata | 53 | cc by PMID 33602937 · DOI · PMC7893044 |
| A phase I/II study of tagraxofusp in Japanese patients with blastic plasmacytoid dendritic cell neoplasm | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 41493719 · DOI · PMC13171773 |
Activated Stat5 trafficking Via Endothelial Cell-derived Extracellular Vesicles Controls IL-3 Pro-angiogenic Paracrine Action [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Soluble factors and cell-derived extracellular vesicles (EVs) control vascular cell fate during inflammation.
- Closing excerpt
- Moreover, these results provide evidence that EC-derived IL-3-EVs can serve as pro-angiogenic clinical delivery wound healing devices.
- 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 (195 words)
Soluble factors and cell-derived extracellular vesicles (EVs) control vascular cell fate during inflammation. The present study investigates the impact of Interleukin 3 (IL-3) on EV release by endothelial cells (ECs), the mechanisms involved in EV release and paracrine actions. We found that IL-3 increases EV release, which is prevented by IL-3Ralpha blockade. EVs released upon IL-3 stimulation were able to induce pro-angiogenic signals as shown by chromatin immunoprecipitation (ChIP) assay performed on the promoter region of cyclin D1 and tridimensional tube-like structure formation. We herein demonstrate that these effects rely on the transfer of miR-126-3p, pre-miR-126 and, more importantly, of activated signal transduction and activator of transcription 5 (pSTAT5) from IL-3-EV cargo into recipient ECs. We show, using the dominant negative form (ΔN)STAT5 and an activated STAT5 (1*6STAT5) constructs, that STAT5 drives IL-3-mediated EV release, miR-126-3p and pSTAT5 content. Finally, using EVs recovered from ΔNSTAT5 expressing ECs, we provide evidence that miR-126-3p and pSTAT5 trafficking is relevant for IL-3-mediated paracrine pro-angiogenic signals. These results indicate that IL-3 regulates EC-EV release, cargo and IL-3 angiogenic paracrine action via STAT5. Moreover, these results provide evidence that EC-derived IL-3-EVs can serve as pro-angiogenic clinical delivery wound healing devices.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 27157262 · DOI · PMC4860593
Innate Immune Modulation by GM-CSF and IL-3 in Health and Disease [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Granulocyte-macrophage colony-stimulating factor (GM-CSF) and inteleukin-3 (IL-3) have long been known as mediators of emergency myelopoiesis, but recent evidence has highlighted their critical role in modulating innate immune effector functions in mice and humans.
- Closing excerpt
- Altogether, characterizing GM-CSF and IL-3 as central mediators of innate immune activation is poised to open new therapeutic avenues for several immune-mediated disorders and define their potential in the context of immunotherapies.
- 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 (189 words)
Granulocyte-macrophage colony-stimulating factor (GM-CSF) and inteleukin-3 (IL-3) have long been known as mediators of emergency myelopoiesis, but recent evidence has highlighted their critical role in modulating innate immune effector functions in mice and humans. This new wealth of knowledge has uncovered novel aspects of the pathogenesis of a range of disorders, including infectious, neoplastic, autoimmune, allergic and cardiovascular diseases. Consequently, GM-CSF and IL-3 are now being investigated as therapeutic targets for some of these disorders, and some phase I/II clinical trials are already showing promising results. There is also pre-clinical and clinical evidence that GM-CSF can be an effective immunostimulatory agent when being combined with anti-cytotoxic T lymphocyte-associated protein 4 (anti-CTLA-4) in patients with metastatic melanoma as well as in novel cancer immunotherapy approaches. Finally, GM-CSF and to a lesser extent IL-3 play a critical role in experimental models of trained immunity by acting not only on bone marrow precursors but also directly on mature myeloid cells. Altogether, characterizing GM-CSF and IL-3 as central mediators of innate immune activation is poised to open new therapeutic avenues for several immune-mediated disorders and define their potential in the context of immunotherapies.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30769926 · DOI · PMC6412223
Interleukin-3 is a predictive marker for severity and outcome during SARS-CoV-2 infections [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a worldwide health threat.
- Closing excerpt
- This study identifies IL-3 as a predictive disease marker for SARS-CoV-2 infections and as a potential therapeutic target for pulmunory viral infections.
- 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 (148 words)
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a worldwide health threat. In a prospective multicentric study, we identify IL-3 as an independent prognostic marker for the outcome during SARS-CoV-2 infections. Specifically, low plasma IL-3 levels is associated with increased severity, viral load, and mortality during SARS-CoV-2 infections. Patients with severe COVID-19 exhibit also reduced circulating plasmacytoid dendritic cells (pDCs) and low plasma IFNα and IFNλ levels when compared to non-severe COVID-19 patients. In a mouse model of pulmonary HSV-1 infection, treatment with recombinant IL-3 reduces viral load and mortality. Mechanistically, IL-3 increases innate antiviral immunity by promoting the recruitment of circulating pDCs into the airways by stimulating CXCL12 secretion from pulmonary CD123+ epithelial cells, both, in mice and in COVID-19 negative patients exhibiting pulmonary diseases. This study identifies IL-3 as a predictive disease marker for SARS-CoV-2 infections and as a potential therapeutic target for pulmunory viral infections.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33602937 · DOI · PMC7893044
A phase I/II study of tagraxofusp in Japanese patients with blastic plasmacytoid dendritic cell neoplasm [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Tagraxofusp (TAG), a first-in-class CD123-targeted therapy, is a recombinant fusion protein of human interleukin-3 conjugated to a truncated diphtheria toxin payload.
- Closing excerpt
- The results indicate that TAG was effective and had a manageable safety profile in Japanese BPDCN patients.
- 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 (198 words)
Tagraxofusp (TAG), a first-in-class CD123-targeted therapy, is a recombinant fusion protein of human interleukin-3 conjugated to a truncated diphtheria toxin payload. Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is an aggressive orphan hematologic cancer with a poor prognosis, and is derived from plasmacytoid dendritic cells that overexpress interleukin-3 receptor subunit alpha (IL3RA or CD123). This open-label phase I/II study evaluated the efficacy and safety of TAG in 11 Japanese BPDCN patients, of whom seven were treatment-naïve (TN) and four had relapsed/refractory (R/R) disease. In the phase I portion, seven patients (five TN, two R/R) were treated, and no dose-limiting toxicity was observed, with 12 μg/kg/day tolerated. In the phase II portion, four patients (two TN, two R/R) were treated. Among the seven TN BPDCN patients, the rate of complete response (CR) + clinical CR (CRc: CR with minimal residual skin abnormality) was 57.1% (90% confidence interval [CI], 22.5-87.1), and the lower limit of the 90% CI (22.5%) exceeded the pre-specified threshold of 10%. Common adverse events included increased alanine aminotransferase (81.8%) and aspartate aminotransferase (72.7%), hypoalbuminemia, hypokalemia, and capillary leak syndrome (54.5%). The results indicate that TAG was effective and had a manageable safety profile in Japanese BPDCN patients.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41493719 · DOI · PMC13171773
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 human hematopoietic colony-stimulating factors [5]
- Research article GM-CSF, IL-3, and IL-5 Family of Cytokines: Regulators of Inflammation [6]
- Research article The GM-CSF/IL-3/IL-5 cytokine receptor family: from ligand recognition to initiation of signaling [7]
- Research article Biology of common beta receptor-signaling cytokines: IL-3, IL-5, and GM-CSF [8]
- Research article Hematopoietic growth factors: ESMO Clinical Practice Guidelines for the applications [9]
- Research article IL-3 signaling and the role of Src kinases, JAKs and STATs: a covert liaison unveiled [10]
References
- Lombardo G, Dentelli P, Togliatto G, Rosso A, Gili M, Gallo S, et al.. Activated Stat5 trafficking Via Endothelial Cell-derived Extracellular Vesicles Controls IL-3 Pro-angiogenic Paracrine Action. . 2016. PMID 27157262 · DOI · PMC4860593
- Borriello F, Galdiero MR, Varricchi G, Loffredo S, Spadaro G, Marone G. Innate Immune Modulation by GM-CSF and IL-3 in Health and Disease. . 2019. PMID 30769926 · DOI · PMC6412223
- Bénard A, Jacobsen A, Brunner M, Krautz C, Klösch B, Swierzy I, et al.. Interleukin-3 is a predictive marker for severity and outcome during SARS-CoV-2 infections. . 2021. PMID 33602937 · DOI · PMC7893044
- Yokota A, Munakata W, Kiguchi T, Ogawa Y, Hino M, Kato K, et al.. A phase I/II study of tagraxofusp in Japanese patients with blastic plasmacytoid dendritic cell neoplasm. . 2026. PMID 41493719 · DOI · PMC13171773
- Clark SC, Kamen R. The human hematopoietic colony-stimulating factors. Science. 1987. PMID 3296190 · DOI
- Dougan M, Dranoff G, Dougan SK. GM-CSF, IL-3, and IL-5 Family of Cytokines: Regulators of Inflammation. Immunity. 2019. PMID 30995500 · DOI · PMC12512237
- Broughton SE, Dhagat U, Hercus TR, Nero TL, Grimbaldeston MA, Bonder CS, et al.. The GM-CSF/IL-3/IL-5 cytokine receptor family: from ligand recognition to initiation of signaling. Immunol Rev. 2012. PMID 23046136 · DOI
- Martinez-Moczygemba M, Huston DP. Biology of common beta receptor-signaling cytokines: IL-3, IL-5, and GM-CSF. J Allergy Clin Immunol. 2003. PMID 14564341 · DOI
- Crawford J, Caserta C, Roila F, ESMO Guidelines Working Group. Hematopoietic growth factors: ESMO Clinical Practice Guidelines for the applications. Ann Oncol. 2010. PMID 20555091 · DOI
- Reddy EP, Korapati A, Chaturvedi P, Rane S. IL-3 signaling and the role of Src kinases, JAKs and STATs: a covert liaison unveiled. Oncogene. 2000. PMID 10851052 · DOI
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.