Evidence map›Paper›PMID 33927210›Full record

ArticleScientific reports2021

Potential impact of celiac disease genetic risk factors on T cell receptor signaling in gluten-specific CD4+ T cells.

Olivier B Bakker, Aarón D Ramírez-Sánchez, Zuzanna A Borek, Niek de Klein, Yang Li, Rutger Modderman, Yvonne Kooy-Winkelaar, Marie K Johannesen, Filomena Matarese, Joost H A Martens and 9 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

3 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
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

19 authors at 5 institutions in 3 countries.

Olivier B Bakker *Department of Genetics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.ORCID https://orcid.org/0000-0002-1447-1327
Aarón D Ramírez-Sánchez *Department of Genetics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.ORCID https://orcid.org/0000-0002-3125-4308
Zuzanna A Borek *Department of Genetics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.ORCID https://orcid.org/0000-0002-7595-6221
Niek de Klein *Department of Genetics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.ORCID https://orcid.org/0000-0003-4640-9904
Yang Li *Department of Genetics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.ORCID https://orcid.org/0000-0003-4022-7341
Rutger ModdermanDepartment of Genetics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Yvonne Kooy-WinkelaarDepartment of Immunohematology and Blood Transfusion, Leiden University Medical Center, Leiden, The Netherlands.
Marie K JohannesenK.G. Jebsen Coeliac Disease Research Centre, Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Filomena MatareseDepartment of Molecular Biology, Nijmegen Centre for Molecular Life Sciences, Radboud University, Nijmegen, The Netherlands.
Joost H A MartensDepartment of Molecular Biology, Nijmegen Centre for Molecular Life Sciences, Radboud University, Nijmegen, The Netherlands.ORCID https://orcid.org/0000-0003-2008-6537
Vinod KumarDepartment of Genetics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.ORCID https://orcid.org/0000-0002-2775-6049
Jeroen van BergenDepartment of Immunohematology and Blood Transfusion, Leiden University Medical Center, Leiden, The Netherlands.
Shuo-Wang QiaoK.G. Jebsen Coeliac Disease Research Centre, Institute of Clinical Medicine, University of Oslo, Oslo, Norway.ORCID https://orcid.org/0000-0002-0935-8397
Knut E A LundinK.G. Jebsen Coeliac Disease Research Centre, Institute of Clinical Medicine, University of Oslo, Oslo, Norway.ORCID https://orcid.org/0000-0003-1713-5545
Ludvig M SollidK.G. Jebsen Coeliac Disease Research Centre, Institute of Clinical Medicine, University of Oslo, Oslo, Norway.ORCID https://orcid.org/0000-0001-8860-704X
Frits KoningDepartment of Immunohematology and Blood Transfusion, Leiden University Medical Center, Leiden, The Netherlands.ORCID http://orcid.org/0000-0002-4007-5715
Cisca WijmengaDepartment of Genetics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.ORCID https://orcid.org/0000-0002-5635-1614
Sebo WithoffDepartment of Genetics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.ORCID https://orcid.org/0000-0001-7704-3437
Iris H JonkersDepartment of Genetics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands. i.h.jonkers@umcg.nl.ORCID https://orcid.org/0000-0003-2304-7939
University Medical Center Groningen · NLOslo University Hospital · NOLeiden University Medical Center · NLRadboud University Nijmegen · NLNitte University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Celiac disease is an auto-immune disease in which an immune response to dietary gluten leads to inflammation and subsequent atrophy of small intestinal villi, causing severe bowel discomfort and malabsorption of nutrients. The major instigating factor for the immune response in celiac disease is the activation of gluten-specific CD4+ T cells expressing T cell receptors that recognize gluten peptides presented in the context of HLA-DQ2 and DQ8. Here we provide an in-depth characterization of 28 gluten-specific T cell clones. We assess their transcriptional and epigenetic response to T cell receptor stimulation and link this to genetic factors associated with celiac disease. Gluten-specific T cells have a distinct transcriptional profile that mostly resembles that of Th1 cells but also express cytokines characteristic of other types of T-helper cells. This transcriptional response appears not to be regulated by changes in chromatin state, but rather by early upregulation of transcription factors and non-coding RNAs that likely orchestrate the subsequent activation of genes that play a role in immune pathways. Finally, integration of chromatin and transcription factor binding profiles suggest that genes activated by T cell receptor stimulation of gluten‑specific T cells may be impacted by genetic variation at several genetic loci associated with celiac disease.

Indexed as

BiomarkersCD4-Positive T-LymphocytesCeliac DiseaseCytokinesGene Expression ProfilingGene Expression RegulationGlutensHumansReceptors, Antigen, T-CellTranscriptomeBiomarkersCytokinesGlutensReceptors, Antigen, T-Cell

Identifiers

PMID33927210
PMCPMC8085175
OpenAlexW3158254944

What OpenQuestion holds

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LicenceCC BY
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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.