Evidence map›Paper›PMID 29520062›Full record

ArticleNature communications2018

The H2B deubiquitinase Usp22 promotes antibody class switch recombination by facilitating non-homologous end joining.

Conglei Li, Thergiory Irrazabal, Clare C So, Maribel Berru, Likun Du, Evelyn Lam, Alexanda K Ling, Jennifer L Gommerman, Qiang Pan-Hammarström, Alberto Martin

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
5.5field-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

43 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Reciprocal regulation of TNF receptor 1-mediated signaling and inflammatory damages by MARCH2 and USP22.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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 2 institutions in 2 countries.

Conglei LiDepartment of Immunology, University of Toronto, Toronto, Ontario, Canada, M5S 1A8.
Thergiory IrrazabalDepartment of Immunology, University of Toronto, Toronto, Ontario, Canada, M5S 1A8.
Clare C SoDepartment of Immunology, University of Toronto, Toronto, Ontario, Canada, M5S 1A8.
Maribel BerruDepartment of Immunology, University of Toronto, Toronto, Ontario, Canada, M5S 1A8.
Likun DuDepartment of Laboratory Medicine, Karolinska Institutet, Stockholm, SE14186, Sweden.
Evelyn LamDepartment of Immunology, University of Toronto, Toronto, Ontario, Canada, M5S 1A8.
Alexanda K LingDepartment of Immunology, University of Toronto, Toronto, Ontario, Canada, M5S 1A8.
Jennifer L GommermanDepartment of Immunology, University of Toronto, Toronto, Ontario, Canada, M5S 1A8.
Qiang Pan-HammarströmDepartment of Laboratory Medicine, Karolinska Institutet, Stockholm, SE14186, Sweden.ORCID http://orcid.org/0000-0003-1990-8804
Alberto MartinDepartment of Immunology, University of Toronto, Toronto, Ontario, Canada, M5S 1A8. alberto.martin@utoronto.ca.
University of Toronto · CAKarolinska Institutet · SE

Funding

KOMP2-Phase3 Production and Phenotyping by the DTCC Consortium TCP Transfer to UC DavisUM1OD023221 · OD · UNIVERSITY OF CALIFORNIA AT DAVIS · PI KC KENT LLOYD · 2016 to 2026
$45.7M
NIH HHS UM1 OD023221
6 · The paper itself

Abstract

Class switch recombination (CSR) has a fundamental function during humoral immune response and involves the induction and subsequent repair of DNA breaks in the immunoglobulin (Ig) switch regions. Here we show the role of Usp22, the SAGA complex deubiquitinase that removes ubiquitin from H2B-K120, in the repair of programmed DNA breaks in vivo. Ablation of Usp22 in primary B cells results in defects in γH2AX and impairs the classical non-homologous end joining (c-NHEJ), affecting both V(D)J recombination and CSR. Surprisingly, Usp22 depletion causes defects in CSR to various Ig isotypes, but not IgA. We further demonstrate that IgG CSR primarily relies on c-NHEJ, whereas CSR to IgA is more reliant on the alternative end joining pathway, indicating that CSR to different isotypes involves distinct DNA repair pathways. Hence, Usp22 is the first deubiquitinase reported to regulate both V(D)J recombination and CSR in vivo by facilitating c-NHEJ.

Indexed as

DNA End-Joining RepairImmunoglobulin Class SwitchingV(D)J RecombinationAnimalsB-LymphocytesDeubiquitinating EnzymesEndopeptidasesFemaleHistonesImmunity, HumoralImmunoglobulin IsotypesMiceMice, Inbred C57BLMice, KnockoutPrimary Cell CultureUbiquitinDeubiquitinating EnzymesEndopeptidasesHistonesImmunoglobulin IsotypesUbiquitinUbiquitin ThiolesteraseUSP22 protein, mouse

Identifiers

PMID29520062
PMCPMC5843634
OpenAlexW2790504889

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.