ArticleGenes and immunity2013
Targeted resequencing identifies defective variants of decoy receptor 3 in pediatric-onset inflammatory bowel disease.
Article in Genes and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 15 citations in OpenAlex.
- Article
- Therapeutic approaches targeting CD95L/CD95 signaling in cancer and autoimmune diseases.Cell death & disease · 2022Review
- Correlation of Serum Decoy Receptor 3 and Interleukin-6 with Severity of Coronary Artery Diseases in Male Acute Myocardial Infarction Patients.Acta bio-medica : Atenei Parmensis · 2021Article
- A catalog of GWAS fine-mapping efforts in autoimmune disease.American journal of human genetics · 2021Review
- Benefits and limitations of genome-wide association studies.Nature reviews. Genetics · 2019Review
- Insights into rheumatic diseases from next-generation sequencing.Nature reviews. Rheumatology · 2019Review
- Up-regulation of DcR3 in microbial toxins-stimulated HUVECs involves NF-κB signalling.BMC biochemistry · 2018Article
- Decoy receptor 3: an endogenous immunomodulator in cancer growth and inflammatory reactions.Journal of biomedical science · 2017Review
- Opportunities and challenges of whole-genome and -exome sequencing.BMC genetics · 2017Review
- The TNF-family cytokine TL1A: from lymphocyte costimulator to disease co-conspirator.Journal of leukocyte biology · 2015Review
- Decoy Receptor 3 Improves Survival in Experimental Sepsis by Suppressing the Inflammatory Response and Lymphocyte Apoptosis.PloS one · 2015Article
- Role of genetics in pediatric inflammatory bowel disease.Inflammatory bowel diseases · 2014Review
- Use of next-generation DNA sequencing to analyze genetic variants in rheumatic disease.Arthritis research & therapy · 2014Review
- Impact of exome sequencing in inflammatory bowel disease.World journal of gastroenterology · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genome-wide association studies have implicated common variation at the 20q13 locus in inflammatory bowel disease, particularly for the pediatric Crohn's form. This locus harbors tumor necrosis factor receptor superfamily (TNFRSF6B), encoding a secreted protein, decoy receptor 3 (DcR3), which binds to and neutralizes pro-inflammatory cytokines of the tumor necrosis factor superfamily. We sought to further the evidence of DcR3's role in pediatric IBD by identifying missense mutations with functional significance within TNFRSF6B. We sequenced the exons of the gene in 528 Caucasian pediatric IBD cases and 549 Caucasian healthy controls to establish the frequency of such events in each population. Sequencing revealed that our IBD cohort harbored a greater number of missense variants, yielding an odds ratio of 3.9 (P-value=0.005). Using functional assays, we established that the frequency of mutants defective in secretion from cultured cells was greater in the Crohn's category than in the controls, yielding an odds ratio of 7.1 (P-value=0.004). These results suggest that rare defective variants in TNFRSF6B have a role in the pathogenesis of some cases of IBD and that interventions targeting this group of tumor necrosis factor-family members may benefit patients with IBD.
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.