Evidence map›Paper›PMID 31036800›Full record

ArticleNature communications2019

FcγRIIb differentially regulates pre-immune and germinal center B cell tolerance in mouse and human.

Marion Espéli, Rachael Bashford-Rogers, John M Sowerby, Nagham Alouche, Limy Wong, Alice E Denton, Michelle A Linterman, Kenneth G C Smith

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
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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

8 authors at 4 institutions in 3 countries.

Marion EspéliThe Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge Biomedical Campus, Cambridge, CB2 OXY, England, UK. marion.espeli@inserm.fr.
Rachael Bashford-RogersThe Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge Biomedical Campus, Cambridge, CB2 OXY, England, UK.
John M SowerbyThe Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge Biomedical Campus, Cambridge, CB2 OXY, England, UK.
Nagham AloucheUMR996 - Inflammation, Chemokines and Immunopathology, Inserm, Univ Paris-Sud, Université Paris-Saclay, Clamart, F-92140, France.
Limy WongThe Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge Biomedical Campus, Cambridge, CB2 OXY, England, UK.
Alice E DentonThe Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge Biomedical Campus, Cambridge, CB2 OXY, England, UK.
Michelle A LintermanThe Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge Biomedical Campus, Cambridge, CB2 OXY, England, UK.ORCID http://orcid.org/0000-0001-6047-1996
Kenneth G C SmithThe Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge Biomedical Campus, Cambridge, CB2 OXY, England, UK. kgcs2@cam.ac.uk.ORCID http://orcid.org/0000-0001-9170-5775
University of Cambridge · GBBabraham Institute · GBInserm · FRCentre for Human Genetics · GB

Funding

Biotechnology and Biological Sciences Research Council BBS/E/B/000C0407Wellcome TrustWellcome Trust 083650/Z/07/ZWellcome Trust 200871/Z/16/Z
6 · The paper itself

Abstract

Several tolerance checkpoints exist throughout B cell development to control autoreactive B cells and prevent the generation of pathogenic autoantibodies. FcγRIIb is an Fc receptor that inhibits B cell activation and, if defective, is associated with autoimmune disease, yet its impact on specific B cell tolerance checkpoints is unknown. Here we show that reduced expression of FcγRIIb enhances the deletion and anergy of autoreactive immature B cells, but in contrast promotes autoreactive B cell expansion in the germinal center and serum autoantibody production, even in response to exogenous, non-self antigens. Our data thus show that FcγRIIb has opposing effects on pre-immune and post-immune tolerance checkpoints, and suggest that B cell tolerance requires the control of bystander germinal center B cells with low or no affinity for the immunizing antigen.

Indexed as

AlgorithmsAnimalsB-LymphocytesCell DifferentiationCell ProliferationEnzyme-Linked Immunosorbent AssayFemaleFlow CytometryGerminal CenterHumansImmune ToleranceLeukocytes, MononuclearMaleMiceReceptors, IgGSoftwareReceptors, IgG

Identifiers

PMID31036800
PMCPMC6488660
OpenAlexW2941068106

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.