Evidence map›Paper›PMID 31285344›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2019

Efficient T cell-B cell collaboration guides autoantibody epitope bias and onset of celiac disease.

Rasmus Iversen, Bishnudeo Roy, Jorunn Stamnaes, Lene S Høydahl, Kathrin Hnida, Ralf S Neumann, Ilma R Korponay-Szabó, Knut E A Lundin, Ludvig M Sollid

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

31 citing papers in PubMed, 55 citations in OpenAlex.

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  13. B cells in human lymphoid structures.Clinical and experimental immunology · 2022
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  19. The Ins and Outs of Antigen Uptake in B cells.Frontiers in immunology · 2022
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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

9 authors at 2 institutions in 3 countries.

Rasmus IversenKG Jebsen Coeliac Disease Research Centre, University of Oslo, NO-0372 Oslo, Norway; rasmus.iversen@medisin.uio.no l.m.sollid@medisin.uio.no.ORCID 0000-0002-3292-1766
Bishnudeo RoyDepartment of Immunology, Oslo University Hospital, NO-0372 Oslo, Norway.
Jorunn StamnaesKG Jebsen Coeliac Disease Research Centre, University of Oslo, NO-0372 Oslo, Norway.
Lene S HøydahlKG Jebsen Coeliac Disease Research Centre, University of Oslo, NO-0372 Oslo, Norway.ORCID 0000-0001-6070-1413
Kathrin HnidaDepartment of Immunology, Oslo University Hospital, NO-0372 Oslo, Norway.
Ralf S NeumannKG Jebsen Coeliac Disease Research Centre, University of Oslo, NO-0372 Oslo, Norway.
Ilma R Korponay-SzabóCeliac Disease Center, Heim Pál National Pediatric Institute, HU-1089 Budapest, Hungary.
Knut E A LundinKG Jebsen Coeliac Disease Research Centre, University of Oslo, NO-0372 Oslo, Norway.
Ludvig M SollidKG Jebsen Coeliac Disease Research Centre, University of Oslo, NO-0372 Oslo, Norway; rasmus.iversen@medisin.uio.no l.m.sollid@medisin.uio.no.
Oslo University Hospital · NOHeim Pál Országos Gyermekgyógyászati Intézet · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

B cells play important roles in autoimmune diseases through autoantibody production, cytokine secretion, or antigen presentation to T cells. In most cases, the contribution of B cells as antigen-presenting cells is not well understood. We have studied the autoantibody response against the enzyme transglutaminase 2 (TG2) in celiac disease patients by generating recombinant antibodies from single gut plasma cells reactive with discrete antigen domains and by undertaking proteomic analysis of anti-TG2 serum antibodies. The majority of the cells recognized epitopes in the N-terminal domain of TG2. Antibodies recognizing C-terminal epitopes interfered with TG2 cross-linking activity, and B cells specific for C-terminal epitopes were inefficient at taking up TG2-gluten complexes for presentation to gluten-specific T cells. The bias toward N-terminal epitopes hence reflects efficient T-B collaboration. Production of antibodies against N-terminal epitopes coincided with clinical onset of disease, suggesting that TG2-reactive B cells with certain epitope specificities could be the main antigen-presenting cells for pathogenic, gluten-specific T cells. The link between B cell epitopes, antigen presentation, and disease onset provides insight into the pathogenic mechanisms of a T cell-mediated autoimmune condition.

Indexed as

Age of OnsetAntigen-Presenting CellsAutoantibodiesAutoantigensB-LymphocytesCeliac DiseaseDuodenumEpitopes, B-LymphocyteGlutensGTP-Binding ProteinsHumansImmune SeraImmunoglobulin Light ChainsModels, MolecularProtein BindingProtein ConformationAutoantibodiesAutoantigensEpitopes, B-LymphocyteGlutensGTP-Binding ProteinsImmune SeraImmunoglobulin Light ChainsProtein Glutamine gamma Glutamyltransferase 2Transglutaminasesantigen presentationautoantibodiesB cellsceliac disease

Identifiers

PMID31285344
PMCPMC6660736
OpenAlexW2957317198

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.