Evidence map›Paper›PMID 33095260›Full record

ArticleThe Journal of experimental medicine2021

Longevity, clonal relationship, and transcriptional program of celiac disease-specific plasma cells.

Ida Lindeman, Chunyan Zhou, Linn M Eggesbø, Zhichao Miao, Justyna Polak, Knut E A Lundin, Jørgen Jahnsen, Shuo-Wang Qiao, Rasmus Iversen, Ludvig M Sollid

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

20 citing papers in PubMed, 47 citations in OpenAlex.

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  11. Celiac disease: mechanisms and emerging therapeutics.Trends in pharmacological sciences · 2023
    Review
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  14. 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

10 authors at 4 institutions in 3 countries.

Ida LindemanKG Jebsen Coeliac Disease Research Centre, University of Oslo, Oslo, Norway.
Chunyan ZhouKG Jebsen Coeliac Disease Research Centre, University of Oslo, Oslo, Norway.
Linn M EggesbøKG Jebsen Coeliac Disease Research Centre, University of Oslo, Oslo, Norway.
Zhichao MiaoEuropean Molecular Biology Laboratory, European Bioinformatics Institute, Wellcome Genome Campus, Cambridge, UK.
Justyna PolakKG Jebsen Coeliac Disease Research Centre, University of Oslo, Oslo, Norway.
Knut E A LundinKG Jebsen Coeliac Disease Research Centre, University of Oslo, Oslo, Norway.
Jørgen JahnsenDepartment of Gastroenterology, Akershus University Hospital, Lørenskog, Norway.
Shuo-Wang QiaoKG Jebsen Coeliac Disease Research Centre, University of Oslo, Oslo, Norway.
Rasmus IversenKG Jebsen Coeliac Disease Research Centre, University of Oslo, Oslo, Norway.
Ludvig M SollidKG Jebsen Coeliac Disease Research Centre, University of Oslo, Oslo, Norway.
Oslo University Hospital · NONanchang University · CNTongji University · CNUniversity of Oslo · NO

Funding

Wellcome TrustWellcome Trust 108437/Z/15/Z
6 · The paper itself

Abstract

Disease-specific plasma cells (PCs) reactive with transglutaminase 2 (TG2) or deamidated gluten peptides (DGPs) are abundant in celiac disease (CeD) gut lesions. Their contribution toward CeD pathogenesis is unclear. We assessed expression of markers associated with PC longevity in 15 untreated and 26 treated CeD patients in addition to 13 non-CeD controls and performed RNA sequencing with clonal inference and transcriptomic analysis of 3,251 single PCs. We observed antigen-dependent V-gene selection and stereotypic antibodies. Generation of recombinant DGP-specific antibodies revealed a key role of a heavy chain residue that displays polymorphism, suggesting that immunoglobulin gene polymorphisms may influence CeD-specific antibody responses. We identified transcriptional differences between CeD-specific and non-disease-specific PCs and between short-lived and long-lived PCs. The short-lived CD19+CD45+ phenotype dominated in untreated and short-term-treated CeD, in particular among disease-specific PCs but also in the general PC population. Thus, the disease lesion of untreated CeD is characterized by massive accumulation of short-lived PCs that are not only directed against disease-specific antigens.

Indexed as

Amino Acid SequenceAnimalsAntibody FormationAntigens, CD19Celiac DiseaseCell LineGene Expression ProfilingGlutensGTP-Binding ProteinsHumansImmunoglobulin AImmunoglobulin Heavy ChainsLeukocyte Common AntigensLongevityPlasma CellsPolymorphism, GeneticAntigens, CD19GlutensGTP-Binding ProteinsImmunoglobulin AImmunoglobulin Heavy ChainsLeukocyte Common AntigensProtein Glutamine gamma Glutamyltransferase 2Transglutaminases

Identifiers

PMID33095260
PMCPMC7590513
OpenAlexW3094437240

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.