Evidence map›Paper›PMID 21700883›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

Activation-induced cytidine deaminase (AID) is required for B-cell tolerance in humans.

Greta Meyers, Yen-Shing Ng, Jason M Bannock, Aubert Lavoie, Jolan E Walter, Luigi D Notarangelo, Sara S Kilic, Guzide Aksu, Marianne Debré, Frédéric Rieux-Laucat and 4 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
6.1field-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

80 citing papers in PubMed, 130 citations in OpenAlex.

  1. Trial
  2. Article
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  4. Distributed Clonal Deletion Prevents Autoimmune Disease Progression.bioRxiv : the preprint server for biology · 2026
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  19. Tracing Self-Reactive B Cells in Normal Mice.Journal of immunology (Baltimore, Md. : 1950) · 2020
    Article
  20. Article

20 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

14 authors at 10 institutions in 4 countries.

Greta MeyersDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06511, USA.
Yen-Shing Ng
Jason M Bannock
Aubert Lavoie
Jolan E Walter
Luigi D Notarangelo
Sara S Kilic
Guzide Aksu
Marianne Debré
Frédéric Rieux-Laucat
Mary Ellen Conley
Charlotte Cunningham-Rundles
Anne Durandy
Eric Meffre
Yale University · USUniversité Paris Cité · FRBursa Uludağ Üni̇versi̇tesi̇ · TRCentre hospitalier de l'Université Laval · CADana-Farber/Boston Children's Cancer and Blood Disorders Center · USEge University · TRHarvard University · USHôpital Necker-Enfants Malades · FRMount Sinai Medical Center · USUniversity of Tennessee Health Science Center · 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
Loss of B Cell Tolerance in Rheumatoid ArthritisR01AI071087 · NIAID · YALE UNIVERSITY · PI MEFFRE, ERIC · 2006 to 2016
$4.3M
Yale Autoimmunity Center of ExcellenceU19AI082713 · NIAID · YALE UNIVERSITY · PI CHO, JUDY H. · 2009 to 2013
$3.6M
Impact of regulatory T cells on human peripheral B cell toleranceR21AI095848 · NIAID · YALE UNIVERSITY · PI MEFFRE, ERIC · 2012 to 2013
$457k
NIAID NIH HHS AI061093NIAID NIH HHS AI071087NIAID NIH HHS AI082713NIAID NIH HHS P01 AI061093NIAID NIH HHS R01 AI071087NIAID NIH HHS R21 AI095848NIAID NIH HHS U19 AI082713
6 · The paper itself

Abstract

Impaired immune functions leading to primary immunodeficiencies often correlate with paradoxical autoimmune complications; patients with hyper-IgM syndromes who are deficient in activation-induced cytidine deaminase (AID), which is required for class-switch recombination and somatic hypermutation, are prone to develop autoimmune diseases. To investigate the impact of AID-deficiency on early B-cell tolerance checkpoints in humans, we tested by ELISA the reactivity of recombinant antibodies isolated from single B cells from AID-deficient patients. New emigrant/transitional and mature naive B cells from AID-deficient patients express an abnormal Ig repertoire and high frequencies of autoreactive antibodies, demonstrating that AID is required for the establishment of both central and peripheral B-cell tolerance. In addition, B-cell tolerance was further breached in AID-deficient patients as illustrated by the detection of anti-nuclear IgM antibodies in the serum of all patients. Thus, we identified a major and previously unsuspected role for AID in the removal of developing autoreactive B cells in humans.

Indexed as

AdolescentAdultAICDA (Activation-Induced Cytidine Deaminase)Amino Acid SequenceAntibodies, AntinuclearB-Cell Activating FactorB-LymphocytesCase-Control StudiesChildChild, PreschoolCytidine DeaminaseFemaleHumansImmunoglobulin MJob SyndromeMaleAICDA (Activation-Induced Cytidine Deaminase)Antibodies, AntinuclearB-Cell Activating FactorCytidine DeaminaseImmunoglobulin MTNFSF13B protein, human

Identifiers

PMID21700883
PMCPMC3136251
OpenAlexW1973389611

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.