Evidence map›Paper›PMID 31591571›Full record

ArticleNature immunology2019

Ikaros prevents autoimmunity by controlling anergy and Toll-like receptor signaling in B cells.

Tanja A Schwickert, Hiromi Tagoh, Karina Schindler, Maria Fischer, Markus Jaritz, Meinrad Busslinger

Open access · greenAbstract read
In one paragraph

Article in Nature immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 7% 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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. IKZF-associated inborn errors of immunity.Journal of human immunity · 2025
    Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
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  17. Article
  18. Article
  19. Article
  20. IKAROS Family Transcription Factors in Lymphocyte Differentiation and Function.Advances in experimental medicine and biology · 2024
    Review
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

6 authors at 1 institution in 2 countries.

Tanja A SchwickertResearch Institute of Molecular Pathology, Vienna Biocenter, Vienna, Austria. tanja.schwickert@imp.ac.at.ORCID http://orcid.org/0000-0002-3371-2376
Hiromi TagohResearch Institute of Molecular Pathology, Vienna Biocenter, Vienna, Austria.ORCID http://orcid.org/0000-0001-9905-6992
Karina SchindlerResearch Institute of Molecular Pathology, Vienna Biocenter, Vienna, Austria.
Maria FischerResearch Institute of Molecular Pathology, Vienna Biocenter, Vienna, Austria.
Markus JaritzResearch Institute of Molecular Pathology, Vienna Biocenter, Vienna, Austria.
Meinrad BusslingerResearch Institute of Molecular Pathology, Vienna Biocenter, Vienna, Austria. meinrad.busslinger@imp.ac.at.ORCID http://orcid.org/0000-0002-9111-9351
Research Institute of Molecular Pathology · AT

Funding

Austrian Science Fund FWF T 838European Research Council 740349
6 · The paper itself

Abstract

The establishment of a diverse B cell antigen receptor (BCR) repertoire by V(D)J recombination also generates autoreactive B cells. Anergy is one tolerance mechanism; it renders autoreactive B cells insensitive to stimulation by self-antigen, whereas Toll-like receptor (TLR) signaling can reactivate anergic B cells. Here, we describe a critical role of the transcription factor Ikaros in controlling BCR anergy and TLR signaling. Mice with specific deletion of Ikaros in mature B cells developed systemic autoimmunity. Ikaros regulated many anergy-associated genes, including Zfp318, which is implicated in the attenuation of BCR responsiveness by promoting immunoglobulin D expression in anergic B cells. TLR signaling was hyperactive in Ikaros-deficient B cells, which failed to upregulate feedback inhibitors of the MyD88-nuclear factor κB signaling pathway. Systemic inflammation was lost on expression of a non-self-reactive BCR or loss of MyD88 in Ikaros-deficient B cells. Thus, Ikaros acts as a guardian preventing autoimmunity by promoting BCR anergy and restraining TLR signaling.

Indexed as

AnimalsAutoimmunityB-LymphocytesClonal AnergyDNA-Binding ProteinsGene Expression RegulationIkaros Transcription FactorImmunoglobulin DMiceModels, AnimalMyeloid Differentiation Factor 88NF-kappa BReceptors, Antigen, B-CellSignal TransductionToll-Like ReceptorsDNA-Binding ProteinsIkaros Transcription FactorImmunoglobulin DMyd88 protein, mouseMyeloid Differentiation Factor 88NF-kappa BReceptors, Antigen, B-CellToll-Like ReceptorsZfp318 protein, mouseZfpn1a1 protein, mouse

Identifiers

PMID31591571
PMCPMC7115902
OpenAlexW2979010135

What OpenQuestion holds

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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.