Evidence map›Paper›PMID 26590315›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2016

The Expression of BAFF Is Controlled by IRF Transcription Factors.

Maria Sjöstrand, Alina Johansson, Lara Aqrawi, Tomas Olsson, Marie Wahren-Herlenius, Alexander Espinosa

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 3 pooled it
3.9field-weighted citation impact, top 6% 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

60 citing papers in PubMed, 3 syntheses or guidelines pooled it, 100 citations in OpenAlex.

  1. Pooled it
  2. Advances in Pathogenesis of Sjögren's Syndrome.Journal of immunology research · 2021
    Pooled it
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  17. Lessons from Animal Models in Sjögren's Syndrome.International journal of molecular sciences · 2023
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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

6 authors at 2 institutions in 2 countries.

Maria SjöstrandUnit of Experimental Rheumatology, Department of Medicine, Center for Molecular Medicine, Karolinska Institutet, SE-171 76 Stockholm, Sweden;
Alina JohanssonUnit of Experimental Rheumatology, Department of Medicine, Center for Molecular Medicine, Karolinska Institutet, SE-171 76 Stockholm, Sweden;
Lara AqrawiBroegelmann Research Laboratory, The Gade Institute, University of Bergen, N-5201 Bergen, Norway; and.ORCID http://orcid.org/0000-0002-3666-842X
Tomas OlssonUnit of Neuroimmunology, Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institutet, SE-171 77 Stockholm, Sweden.
Marie Wahren-HerleniusUnit of Experimental Rheumatology, Department of Medicine, Center for Molecular Medicine, Karolinska Institutet, SE-171 76 Stockholm, Sweden;ORCID http://orcid.org/0000-0002-0915-7245
Alexander EspinosaUnit of Experimental Rheumatology, Department of Medicine, Center for Molecular Medicine, Karolinska Institutet, SE-171 76 Stockholm, Sweden; alexander.espinosa@ki.se.
Karolinska Institutet · SEUniversity of Bergen · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Patients with systemic lupus erythematosus (SLE) and primary Sjögren's syndrome (pSS) are typically characterized by the presence of autoantibodies and an IFN-signature. The strength of the IFN-signature positively correlates with disease severity, suggesting that type I IFNs are active players in these diseases. BAFF is a cytokine critical for development and proper selection of B cells, and the targeting of BAFF has emerged as a successful treatment strategy of SLE. Previous reports have suggested that BAFF expression is directly induced by type I IFNs, but the precise mechanism for this remains unknown. In this article, we demonstrate that BAFF is a bona fide ISG and that IFN regulatory factors (IRFs) control the expression of BAFF. We identify IRF1 and IRF2 as positive regulators of BAFF transcription and IRF4 and IRF8 as potent repressors; in addition, we have mapped the precise binding site for these factors in the BAFF promoter. IFN-β injections induced BAFF expression mainly in neutrophils and monocytes, and BAFF expression in neutrophils from pSS patients strongly correlated with the strength of the IFN-signature. In summary, we show that BAFF expression is directly induced by type I IFNs via IRF1 and IRF2, whereas IRF4 and IRF8 are negative regulators of BAFF expression. These data suggest that type I IFN blockade in SLE and pSS patients will lead to downregulation of BAFF and a consequential reduction of autoreactive B cell clones and autoantibodies.

Indexed as

AutoantibodiesBase SequenceB-Cell Activating FactorBinding SitesB-LymphocytesCells, CulturedFemaleHumansInterferon-betaInterferon Regulatory Factor-1Interferon Regulatory Factor-2Interferon Regulatory Factor-4Interferon Regulatory Factor-8Interferon Regulatory FactorsLupus Erythematosus, SystemicMaleAutoantibodiesB-Cell Activating FactorInterferon-betaInterferon Regulatory Factor-1Interferon Regulatory Factor-2Interferon Regulatory Factor-4Interferon Regulatory Factor-8Interferon Regulatory FactorsIRF1 protein, humanIRF2 protein, humanTNFSF13B protein, human

Identifiers

PMID26590315
PMCPMC4683359
OpenAlexW2173545185

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.