Evidence map›Paper›PMID 30593798›Full record

ArticleGastroenterology2019

Plasma Cells Are the Most Abundant Gluten Peptide MHC-expressing Cells in Inflamed Intestinal Tissues From Patients With Celiac Disease.

Lene Støkken Høydahl, Lisa Richter, Rahel Frick, Omri Snir, Kristin Støen Gunnarsen, Ole J B Landsverk, Rasmus Iversen, Jeliazko R Jeliazkov, Jeffrey J Gray, Elin Bergseng and 8 more

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

Article in Gastroenterology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
7.2field-weighted citation impact, top 2% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 90 citations in OpenAlex.

  1. Evaluation of ICARUS Guidelines and Recommendations Not Supported by Randomized Controlled Trials.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2023
    Pooled it
  2. Trial
  3. Trial
  4. Review
  5. Review
  6. IFN-γ is a direct driver of crypt hyperplasia in celiac disease.The Journal of clinical investigation · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Celiac disease: mechanisms and emerging therapeutics.Trends in pharmacological sciences · 2023
    Review
  14. Article
  15. Article
  16. 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

18 authors at 3 institutions in 2 countries.

Lene Støkken HøydahlCentre for Immune Regulation and Department of Immunology, University of Oslo and Oslo University Hospital, Oslo, Norway; Centre for Immune Regulation and Department of Biosciences, University of Oslo, Oslo, Norway; KG Jebsen Coeliac Disease Research Centre, University of Oslo, Oslo, Norway. Electronic address: l.s.hoydahl@medisin.uio.no.
Lisa RichterCentre for Immune Regulation and Department of Pathology, University of Oslo and Oslo University Hospital, Oslo, Norway.
Rahel FrickCentre for Immune Regulation and Department of Immunology, University of Oslo and Oslo University Hospital, Oslo, Norway; Centre for Immune Regulation and Department of Biosciences, University of Oslo, Oslo, Norway.
Omri SnirCentre for Immune Regulation and Department of Immunology, University of Oslo and Oslo University Hospital, Oslo, Norway.
Kristin Støen GunnarsenCentre for Immune Regulation and Department of Immunology, University of Oslo and Oslo University Hospital, Oslo, Norway; Centre for Immune Regulation and Department of Biosciences, University of Oslo, Oslo, Norway.
Ole J B LandsverkCentre for Immune Regulation and Department of Pathology, University of Oslo and Oslo University Hospital, Oslo, Norway.
Rasmus IversenCentre for Immune Regulation and Department of Immunology, University of Oslo and Oslo University Hospital, Oslo, Norway.
Jeliazko R JeliazkovProgram in Molecular Biophysics, Johns Hopkins University, Baltimore, Maryland.
Jeffrey J GrayProgram in Molecular Biophysics, Johns Hopkins University, Baltimore, Maryland; Department of Chemical and Biomolecular Engineering and Institute of NanoBioTechnology, Johns Hopkins University, Baltimore, Maryland; Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, Maryland.
Elin BergsengCentre for Immune Regulation and Department of Immunology, University of Oslo and Oslo University Hospital, Oslo, Norway.
Stian FossCentre for Immune Regulation and Department of Immunology, University of Oslo and Oslo University Hospital, Oslo, Norway; Centre for Immune Regulation and Department of Biosciences, University of Oslo, Oslo, Norway.
Shuo-Wang QiaoCentre for Immune Regulation and Department of Immunology, University of Oslo and Oslo University Hospital, Oslo, Norway; KG Jebsen Coeliac Disease Research Centre, University of Oslo, Oslo, Norway.
Knut E A LundinCentre for Immune Regulation and Department of Immunology, University of Oslo and Oslo University Hospital, Oslo, Norway; Department of Gastroenterology, Oslo University Hospital-Rikshospitalet Oslo, Norway.
Jørgen JahnsenDepartment of Gastroenterology, Akershus University Hospital, Lørenskog, Norway; Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Frode L JahnsenCentre for Immune Regulation and Department of Pathology, University of Oslo and Oslo University Hospital, Oslo, Norway.
Inger SandlieCentre for Immune Regulation and Department of Immunology, University of Oslo and Oslo University Hospital, Oslo, Norway; Centre for Immune Regulation and Department of Biosciences, University of Oslo, Oslo, Norway.
Ludvig M SollidCentre for Immune Regulation and Department of Immunology, University of Oslo and Oslo University Hospital, Oslo, Norway; KG Jebsen Coeliac Disease Research Centre, University of Oslo, Oslo, Norway.
Geir Åge LøsetCentre for Immune Regulation and Department of Immunology, University of Oslo and Oslo University Hospital, Oslo, Norway; Centre for Immune Regulation and Department of Biosciences, University of Oslo, Oslo, Norway; Nextera AS, Oslo, Norway. Electronic address: g.a.loset@ibv.uio.no.
Oslo University Hospital · NOJohns Hopkins University · USUniversity of Oslo · NO

Funding

Prediction of the Structure of Therapeutic Antibodies with their AntigensR01GM078221 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI GRAY, JEFFREY J · 2006 to 2020
$4.0M
Computational Design of Crystal Lattice Interactions to Determine Recalcitrant Protein StructuresF31GM123616 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI JELIAZKOV, JELIAZKO · 2017 to 2018
$81k
NIGMS NIH HHS F31 GM123616NIGMS NIH HHS R01 GM078221
6 · The paper itself

Abstract

BACKGROUND &

aimsDevelopment of celiac disease is believed to involve the transglutaminase-dependent response of CD4

methodsWe generated monoclonal antibodies (mAbs) specific for the peptide-MHC (pMHC) complex of HLA-DQ2.5 and the immunodominant gluten epitope DQ2.5-glia-α1a using phage display. We used these mAbs to assess gluten peptide presentation and phenotypes of presenting cells by flow cytometry and enzyme-linked immune absorbent spot (ELISPOT) in freshly prepared single-cell suspensions from intestinal biopsies from 40 patients with celiac disease (35 untreated and 5 on a gluten-free diet) as well as 18 subjects with confirmed noninflamed gut mucosa (controls, 12 presumed healthy, 5 undergoing pancreatoduodenectomy, and 1 with potential celiac disease).

resultsUsing the mAbs, we detected MHC complexes on cells from intestinal biopsies from patients with celiac disease who consume gluten, but not from patients on gluten-free diets. We found B cells and plasma cells to be the most abundant cells that present DQ2.5-glia-α1a in the inflamed mucosa. We identified a subset of plasma cells that expresses B-cell receptors (BCR) specific for gluten peptides or the autoantigen transglutaminase 2 (TG2). Expression of MHC class II (MHCII) was not restricted to these specific plasma cells in patients with celiac disease but was observed in an average 30% of gut plasma cells from patients and controls.

conclusionsA population of plasma cells from intestinal biopsies of patients with celiac disease express MHCII; this is the most abundant cell type presenting the immunodominant gluten peptide DQ2.5-glia-α1a in the tissues from these patients. These results indicate that plasma cells in the gut can function as antigen-presenting cells and might promote and maintain intestinal inflammation in patients with celiac disease or other inflammatory disorders.

Indexed as

Immunity, MucosalImmunodominant EpitopesAnimalsAntigen-Presenting CellsCase-Control StudiesCeliac DiseaseCell LineDiet, Gluten-FreeDuodenumGlutensGTP-Binding ProteinsHLA-DQ AntigensHumansIntestinal MucosaMicePeptide FragmentsGlutensGTP-Binding ProteinsHLA-DQ2 antigenHLA-DQ AntigensImmunodominant EpitopesPeptide FragmentsProtein Glutamine gamma Glutamyltransferase 2TransglutaminasesAPCAutoimmunityImmune ActivationTG2

Identifiers

PMID30593798
PMCPMC6441630
OpenAlexW2905625932

What OpenQuestion holds

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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.