ArticleGenes and immunity2020
Genomic profiling of intestinal T-cell receptor repertoires in inflammatory bowel disease.
Article in Genes and immunity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
The trial behind it
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Challenges in IBD Research 2024: Precision Medicine.Inflammatory bowel diseases · 2024Review
- Novel long non-coding RNAs of relevance for ulcerative colitis pathogenesis.Non-coding RNA research · 2022Article
- Reduced diversity of intestinal T-cell receptor repertoire in patients with Crohn's disease.Frontiers in cellular and infection microbiology · 2022Article
- Heterogeneity of CD4Frontiers in cell and developmental biology · 2020Article
- Circulating α4β7Clinical and experimental gastroenterology · 2020Article
- T Cell Repertoire During Ontogeny and Characteristics in Inflammatory Disorders in Adults and Childhood.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Growing evidence shows that inflammatory bowel disease (IBD) results from dysregulation of immune responses to gut microbes. T-cell receptors (TCRs) expressed on the T-cell surface play critical roles in discriminating pathogens from commensal intestinal microorganisms at the front line of the adaptive immune system. The breakdown of this interaction may trigger persistent inflammatory responses to gut bacteria, resulting in IBD. Taking advantage of high-throughput sequencing, we developed an integrated approach to dissect the intestinal TCR repertoires underlying IBD by collecting peripheral blood and inflamed intestine from the same set of 11 IBD cases. The intestinal TCR repertoires show lower clonotype diversity (p < 0.05) and stronger clonal expansion (p < 0.02) than those in the blood. This pattern becomes more profound in TCRs unique to the inflamed tissue compared with shared TCRs. Our approach further identified the increased usage of TRAV12-3 (false discovery rate, FDR < 5%), which biases its choices of J genes towards the reduction of TRAJ37 and TRAJ43 usage (FDR < 20%) in the inflamed intestine. Our genomic profiling suggests that this selective bias of V and J gene usage may lead to a loss of diversity in the intestinal TCR repertoires and result in mucosal inflammation in IBD.
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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.