ArticleInflammatory bowel diseases2019
Genetic and Transcriptomic Variation Linked to Neutrophil Granulocyte-Macrophage Colony-Stimulating Factor Signaling in Pediatric Crohn's Disease.
Article in Inflammatory bowel diseases, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Review
- Emergency granulopoiesis and innate immune memory in inflammatory bowel disease.Trends in immunology · 2026Review
- Neutrophils at the Crossroads of Inflammatory Bowel Disease and Atherosclerosis: A State-of-the-Art Review.Cells · 2025Review
- Neutrophils in inflammatory bowel disease: disease-promoting versus protective functions.Frontiers in immunology · 2025Review
- Multiomics Integration and Machine Learning Reveal Colony Stimulating Factor 3 Receptor as a Key Gene and Therapeutic Target in Crohn's Disease.Mediators of inflammation · 2025Article
- Intestinal stroma guides monocyte differentiation to macrophages through GM-CSF.Nature communications · 2024Article
- NOD2 modulates immune tolerance via the GM-CSF-dependent generation of CD103Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- GM-CSF: A Promising Target in Inflammation and Autoimmunity.ImmunoTargets and therapy · 2020Review
- Neutrophil GM-CSF signaling in inflammatory bowel disease patients is influenced by non-coding genetic variants.Scientific reports · 2019Article
- Roles of GM-CSF in the Pathogenesis of Autoimmune Diseases: An Update.Frontiers in immunology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
34 authors at 17 institutions in 2 countries.
Funding
Abstract
backgroundGranulocyte-macrophage colony-stimulating factor auto-antibodies (GMAbs) suppress neutrophil-extrinsic GM-CSF signaling and increase risk for stricturing behavior in Crohn's disease (CD). We aimed to define clinical, genomic, and functional associations with neutrophil-intrinsic GM-CSF signaling.
methodsMissense mutations in CSF2RA, CSF2RB, JAK2, STAT5A, and STAT5B were identified using whole-exome sequencing in 543 pediatric inflammatory bowel disease (IBD) patients. Neutrophil-intrinsic GM-CSF signaling was defined using the GM-CSF-induced STAT5 stimulation index (GMSI) in 180 pediatric IBD patients and 26 non-IBD controls. Reduced GM-CSF signaling (GMSI-Lo) was defined as the 20th percentile within the control group. Variation in neutrophil phospho-protein abundance, bacterial killing, and the global pattern of gene expression with the GMSI was determined.
resultsWe validated 18 potentially damaging missense mutations in CSF2RA and CSF2RB. CSF2RA A17G carriage increased from 10% in those with intact neutrophil GMSI to 32% in those with low GMSI (P = 0.02). The frequency of reduced Staphylococcus aureus killing increased from 17% in those with intact neutrophil GMSI to 35% in GMSI-Lo neutrophils (P = 0.043). Crohn's disease neutrophils with low GMSI exhibited specific alterations in phospho-protein networks and genes regulating cytokine production, wound healing, and cell survival and proliferation. Stricturing behavior increased from 7% in patients with both low GMAb and intact GMSI to 64% in patients with both elevated GMAb and low GMSI (P < 0.0001).
conclusionsLow/normal neutrophil-intrinsic GM-CSF signaling is associated with CSF2RA missense mutations, alterations in gene expression networks, and higher rates of disease complications in pediatric CD.
Indexed as
Identifiers
What OpenQuestion holds
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.