Evidence map›Paper›PMID 32265907›Full record

ArticleFrontiers in immunology2020

In Human Autoimmunity, a Substantial Component of the B Cell Repertoire Consists of Polyclonal, Barely Mutated IgG

Graeme J M Cowan, Katherine Miles, Lorenzo Capitani, Sophie S B Giguere, Hanna Johnsson, Carl Goodyear, Iain B McInnes, Steffen Breusch, David Gray, Mohini Gray

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 28 citations in OpenAlex.

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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 5 institutions in 2 countries.

Graeme J M CowanAshworth Laboratories, School of Biological Sciences, Institute of Immunology and Infection Research, The University of Edinburgh, Edinburgh, United Kingdom.
Katherine MilesMRC/University of Edinburgh Centre for Inflammation Research, The Queen's Medical Research Institute, Edinburgh, United Kingdom.
Lorenzo CapitaniAshworth Laboratories, School of Biological Sciences, Institute of Immunology and Infection Research, The University of Edinburgh, Edinburgh, United Kingdom.
Sophie S B GiguereAshworth Laboratories, School of Biological Sciences, Institute of Immunology and Infection Research, The University of Edinburgh, Edinburgh, United Kingdom.
Hanna JohnssonCollege of Medical, Veterinary and Life Sciences, Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, United Kingdom.
Carl GoodyearCollege of Medical, Veterinary and Life Sciences, Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, United Kingdom.
Iain B McInnesCollege of Medical, Veterinary and Life Sciences, Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, United Kingdom.
Steffen BreuschOrthopaedic Unit, Royal Infirmary of Edinburgh, Edinburgh, United Kingdom.
David GrayAshworth Laboratories, School of Biological Sciences, Institute of Immunology and Infection Research, The University of Edinburgh, Edinburgh, United Kingdom.
Mohini GrayMRC/University of Edinburgh Centre for Inflammation Research, The Queen's Medical Research Institute, Edinburgh, United Kingdom.
University of Edinburgh · GBUniversity of Glasgow · GBCentre for Inflammation Research · GBEdinburgh Royal Infirmary · GBHarvard University · US

Funding

Wellcome TrustWellcome Trust WT109705MA
6 · The paper itself

Abstract

B cells are critical for promoting autoimmunity and the success of B cell depletion therapy in rheumatoid arthritis (RA) confirms their importance in driving chronic inflammation. Whilst disease specific autoantibodies are useful diagnostically, our understanding of the pathogenic B cell repertoire remains unclear. Defining it would lead to novel insights and curative treatments. To address this, we have undertaken the largest study to date of over 150 RA patients, utilizing next generation sequencing (NGS) to analyze up to 200,000 BCR sequences per patient. The full-length antigen-binding variable region of the heavy chain (IgGHV) of the IgG B cell receptor (BCR) were sequenced. Surprisingly, RA patients do not express particular clonal expansions of B cells at diagnosis. Rather they express a polyclonal IgG repertoire with a significant increase in BCRs that have barely mutated away from the germline sequence. This pattern remains even after commencing disease modifying therapy. These hypomutated BCRs are expressed by TNF-alpha secreting IgG

Indexed as

AutoimmunityGenes, ImmunoglobulinAntirheumatic AgentsArthritis, RheumatoidAutoantibodiesB-LymphocytesCell LineageClone CellsHigh-Throughput Nucleotide SequencingHumansImmunoglobulin GImmunoglobulin Heavy ChainsImmunoglobulin Variable RegionLymphocyte ActivationLymphocyte SubsetsReceptors, Antigen, B-CellAntirheumatic AgentsAutoantibodiesImmunoglobulin GImmunoglobulin Heavy ChainsImmunoglobulin Variable RegionReceptors, Antigen, B-CellTumor Necrosis Factor-alphaTumor Necrosis Factor Receptor Superfamily, Member 7autoimmunityB cellsBCRrheumatoid arthritisTNF

Identifiers

PMID32265907
PMCPMC7099054
OpenAlexW3011821586

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.