ArticleBlood2007
Functional deficiencies of granulocyte-macrophage colony stimulating factor and interleukin-3 contribute to insulitis and destruction of beta cells.
Article in Blood, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
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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
21 citing papers in PubMed, 30 citations in OpenAlex.
- GM-CSF promotes pro-inflammatory macrophage activation associated with Akt/mTOR signaling during experimental colitis.Frontiers in immunology · 2026Article
- Role of Interleukins in Type 1 and Type 2 Diabetes.Diagnostics (Basel, Switzerland) · 2025Review
- Review
- IL-3: key orchestrator of inflammation.Frontiers in immunology · 2024Review
- Role of GM-CSF in lung balance and disease.Frontiers in immunology · 2023Review
- The Influence of Different Types of Diabetes on Vascular Complications.Journal of diabetes research · 2022Review
- The involvement of GM-CSF deficiencies in parallel pathways of pulmonary alveolar proteinosis and the alcoholic lung.Alcohol (Fayetteville, N.Y.) · 2019Review
- Review
- The Pleiotropic Effects of the GM-CSF Rheostat on Myeloid Cell Differentiation and Function: More Than a Numbers Game.Frontiers in immunology · 2019Review
- A GMCSF-Neuroantigen Tolerogenic Vaccine Elicits Systemic Lymphocytosis of CD4Frontiers in immunology · 2018Article
- Article
- Article
- GM-CSF-neuroantigen fusion proteins reverse experimental autoimmune encephalomyelitis and mediate tolerogenic activity in adjuvant-primed environments: association with inflammation-dependent, inhibitory antigen presentation.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Microbiota-dependent crosstalk between macrophages and ILC3 promotes intestinal homeostasis.Science (New York, N.Y.) · 2014Article
- Self-antigen presentation by dendritic cells in autoimmunity.Frontiers in immunology · 2014Review
- Cytokine-neuroantigen fusion proteins as a new class of tolerogenic, therapeutic vaccines for treatment of inflammatory demyelinating disease in rodent models of multiple sclerosis.Frontiers in immunology · 2012Article
- Article
- Cellular therapies supplement: the role of granulocyte macrophage colony-stimulating factor and dendritic cells in regulatory T-cell homeostasis and expansion.Transfusion · 2011Article
- A dual role for the immune response in a mouse model of inflammation-associated lung cancer.The Journal of clinical investigation · 2011Article
- Cytokine gene-mediated immunotherapy: current status and future perspectives.Cancer science · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenesis of type 1 diabetes (T1D) involves the immune-mediated destruction of insulin-producing beta cells in the pancreatic islets of Langerhans. Genetic analysis of families with a high incidence of T1D and nonobese diabetic (NOD) mice, a prototypical model of the disorder, uncovered multiple susceptibility loci, although most of the underlying immune defects remain to be delineated. Here we report that aged mice doubly deficient in granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-3 (IL-3) manifest insulitis, destruction of insulin-producing beta cells, and compromised glucose homeostasis. Macrophages from mutant mice produce increased levels of p40 after LPS stimulation, whereas concurrent ablation of interferon-gamma (IFN-gamma) ameliorates the disease. The administration of antibodies that block cytotoxic T lymphocyte associated antigen-4 (CTLA-4) to young mutant mice precipitates the onset of insulitis and hyperglycemia. These results, together with previous reports of impaired hematopoietic responses to GM-CSF and IL-3 in patients with T1D and in NOD mice, indicate that functional deficiencies of these cytokines contribute to diabetes.
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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.