Evidence map›Paper›PMID 29988119›Full record

ArticleMucosal immunology2018

Expanded TCRβ CDR3 clonotypes distinguish Crohn's disease and ulcerative colitis patients.

J Wu, A H Pendegraft, M Byrne-Steele, Q Yang, C Wang, W Pan, T Lucious, T Seay, X Cui, C O Elson and 2 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Mucosal immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.8field-weighted citation impact, top 14% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Challenges in IBD Research 2024: Precision Medicine.Inflammatory bowel diseases · 2024
    Review
  6. Identification of a unique subset of tissue-resident memory CD4Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 3 institutions in 1 country.

J WuDivision of Gastroenterology and Hepatology, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA.
A H PendegraftDepartment of Biostatistics, School of Public Health, University of Alabama at Birmingham, Birmingham, AL, USA.
M Byrne-SteeleiRepertoire, HudsonAlpha Institute, Huntsville, AL, USA.
Q YangiRepertoire, HudsonAlpha Institute, Huntsville, AL, USA.
C WangiRepertoire, HudsonAlpha Institute, Huntsville, AL, USA.
W PaniRepertoire, HudsonAlpha Institute, Huntsville, AL, USA.
T LuciousDivision of Gastroenterology and Hepatology, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA.
T SeayDivision of Gastroenterology and Hepatology, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA.
X CuiDepartment of Biostatistics and Bioinformatics, Rollins School of Public Health, Emory University, Atlanta, GA, USA.
C O ElsonDivision of Gastroenterology and Hepatology, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA.
J HaniRepertoire, HudsonAlpha Institute, Huntsville, AL, USA.
P J MannonDivision of Gastroenterology and Hepatology, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA. pmannon@uabmc.edu.
University of Alabama at Birmingham · USiRepertoire (United States) · USEmory University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We aimed to determine whether the TCR repertoires of Crohn's disease (CD) patients contain highly prevalent disease-specific T-cell clonotypes reflective of the characteristic and highly shared aberrant serum antibody reactivity to gut commensal flagellin antigens. The CD4 TCRβ CDR3 sequence repertoires from active CD (n = 20) and ulcerative colitis (UC) (n = 10) patients were significantly more diverse, and individual sequences over-represented, compared to healthy controls (HC) (n = 97). While a very small number of expanded public CDR3 sequences are highly shared between active CD and UC, the majority of significantly expanded TCRβ CDR3 clonotypes are private to CD and UC patients with equivalent prevalence among IBD patients. Further defining TCR clonotypes by Vβ-CDR3 linkage showed significant differences in the TCR repertoires between UC and CD. Flagellin antigen exposure induced expansion of several TCRβ CDR3 sequences in CD4 cells from a flagellin-seropositive subject including sequences highly shared by or relatively private to CD (and UC) patients. These data suggest that flagellin-reactivity contributes to the expansion of a small number of CD4 clonotypes but does not support flagellin antigens as predominantly driving CD4 cell proliferation in CD. Disease-specific expanded TCRβ CDR3 clonotypes characterize CD and UC and the shared exposure to the gamut of gut microbial antigens.

Indexed as

AntigensCD4-Positive T-LymphocytesCell LineCell ProliferationColitis, UlcerativeCrohn DiseaseFlagellinHumansLeukocytes, MononuclearReceptors, Antigen, T-Cell, alpha-betaAntigensFlagellinReceptors, Antigen, T-Cell, alpha-beta

Identifiers

PMID29988119
OpenAlexW2864684743

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.