Evidence map›Paper›PMID 31721234›Full record

ReviewImmunological reviews2019

Impaired B-cell tolerance checkpoints promote the development of autoimmune diseases and pathogenic autoantibodies.

Eric Meffre, Kevin C O'Connor

Open access · greenAbstract readReview
In one paragraph

Review in Immunological reviews, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

106 citing papers in PubMed, 151 citations in OpenAlex.

  1. Article
  2. Article
  3. β1 Autoantibodies Stimulate T Cells to Become Cardiotoxic.JACC. Basic to translational science · 2026
    Article
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  19. Article
  20. Importance of B cells (Review).International journal of molecular medicine · 2026
    Review

46 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Eric MeffreDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT, USA.ORCID 0000-0003-4326-0171
Kevin C O'ConnorDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT, USA.ORCID 0000-0002-7056-419X
Yale University · US

Funding

Regulation of IgA class switching in the intestinal mucosaP01AI061093 · NIAID · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI CUNNINGHAM-RUNDLES, CHARLOTTE · 2004 to 2021
$29.8M
Rare Disease Network for Myasthenia GravisU54NS115054 · NINDS · GEORGE WASHINGTON UNIVERSITY · PI HENRY J KAMINSKI · 2019 to 2026
$11.9M
Mechanisms of autoimmunity in myasthenia gravisR01AI114780 · NIAID · YALE UNIVERSITY · PI Kevin C O'Connor · 2016 to 2026
$4.7M
Loss of B Cell Tolerance in Rheumatoid ArthritisR01AI071087 · NIAID · YALE UNIVERSITY · PI MEFFRE, ERIC · 2006 to 2016
$4.3M
Mechanisms of autoantibody production in myasthenia gravisR56AI114780 · NIAID · YALE UNIVERSITY · PI O'CONNOR, KEVIN C · 2015 to 2015
$416k
Novel Approaches for Investigating the Pathology of Myasthenia Gravis AutoantibodiesR21AI142198 · NIAID · YALE UNIVERSITY · PI O'CONNOR, KEVIN C · 2019 to 2020
$395k
National Institute of Allergy and Infectious Diseases AI061093National Institute of Allergy and Infectious Diseases AI071087National Institute of Allergy and Infectious Diseases AI114780National Institute of Allergy and Infectious Diseases AI142198National Institute of Neurological Diseases and Stroke NS115054NIAID NIH HHS P01 AI061093NIAID NIH HHS R01 AI071087NIAID NIH HHS R01 AI114780NIAID NIH HHS R21 AI142198NIAID NIH HHS R56 AI114780NINDS NIH HHS U54 NS115054
6 · The paper itself

Abstract

A role for B cells in autoimmune diseases is now clearly established both in mouse models and humans by successful treatment of multiple sclerosis and rheumatoid arthritis with anti-CD20 monoclonal antibodies that eliminate B cells. However, the underlying mechanisms by which B cells promote the development of autoimmune diseases remain poorly understood. Here, we review evidence that patients with autoimmune disease suffer from defects in early B-cell tolerance checkpoints and therefore fail to counterselect developing autoreactive B cells. These B-cell tolerance defects are primary to autoimmune diseases and may result from altered B-cell receptor signaling and dysregulated T-cell/regulatory T-cell compartment. As a consequence, large numbers of autoreactive naive B cells accumulate in the blood of patients with autoimmune diseases and may promote autoimmunity through the presentation of self-antigen to T cells. In addition, new evidence suggests that this reservoir of autoreactive naive B cells contains clones that may develop into CD27

Indexed as

AnimalsAutoantibodiesAutoantigensAutoimmune DiseasesAutoimmunityB-LymphocytesHumansImmune ToleranceLymphocyte ActivationAutoantibodiesAutoantigensautoantibodiesautoimmune diseaseB-cell developmentimmune tolerance checkpoint

Identifiers

PMID31721234
PMCPMC9145185
OpenAlexW2988118358

What OpenQuestion holds

Textmetadata
LicenceTDM
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.