Evidence map›Paper›PMID 25645456›Full record

ArticleEuropean journal of immunology2015

B cells expressing IFN-γ suppress Treg-cell differentiation and promote autoimmune experimental arthritis.

Susan A Olalekan, Yanxia Cao, Keith M Hamel, Alison Finnegan

Open access · bronzeAbstract read
In one paragraph

Article in European journal of immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

61 citing papers in PubMed, 102 citations in OpenAlex.

  1. Article
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  9. IFN-γ-induced Th1-Treg polarization in inflamed brains limits exacerbation of experimental autoimmune encephalomyelitis.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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  12. Review
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  19. Review
  20. IFN-γ and TGF-β, Crucial Players in Immune Responses: A Tribute to Howard Young.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2022
    Review

1 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

4 authors at 2 institutions in 1 country.

Susan A OlalekanDepartment of Immunology/Microbiology, Rush University Medical Center, Cohn Research Building, Chicago, IL, USA.
Yanxia Cao
Keith M Hamel
Alison Finnegan
Rush University Medical Center · USUniversity of Chicago · US

Funding

B CELL FUNCTION IN AUTOIMMUNE ARTHRITISR01AR047657 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI FINNEGAN, ALISON · 2002 to 2011
$3.0M
NIAMS NIH HHS AR047657NIAMS NIH HHS R01 AR047657
6 · The paper itself

Abstract

Clinical efficacy in the treatment of rheumatoid arthritis with anti-CD20 (Rituximab)-mediated B-cell depletion has garnered interest in the mechanisms by which B cells contribute to autoimmunity. We have reported that B-cell depletion in a murine model of proteoglycan-induced arthritis (PGIA) leads to an increase in Treg cells that correlate with decreased autoreactivity. Here, we demonstrate that the increase in Treg cells after B-cell depletion is due to an increase in the differentiation of naïve CD4(+) T cells into Treg cells. Since the development of PGIA is dependent on IFN-γ and B cells are reported to produce IFN-γ, we hypothesized that B-cell-specific IFN-γ plays a role in the development of PGIA. Accordingly, mice with B-cell-specific IFN-γ deficiency were as resistant to the induction of PGIA as mice that were completely IFN-γ deficient. Importantly, despite a normal frequency of IFN-γ-producing CD4(+) T cells, B-cell-specific IFN-γ-deficient mice exhibited a higher percentage of Treg cells compared with that in WT mice. These data indicate that B-cell IFN-γ production inhibits Treg-cell differentiation and exacerbates arthritis. Thus, we have established that IFN-γ, specifically derived from B cells, uniquely contributes to the pathogenesis of autoimmunity through prevention of immunoregulatory mechanisms.

Indexed as

Lymphocyte DepletionAdjuvants, ImmunologicAggrecansAnimalsAntibodies, Monoclonal, Murine-DerivedArthritis, ExperimentalArthritis, RheumatoidB-LymphocytesCell DifferentiationCell ProliferationCells, CulturedCytokinesForkhead Transcription FactorsInterferon-gammaLymphocyte ActivationMiceAdjuvants, ImmunologicAggrecansAntibodies, Monoclonal, Murine-DerivedCytokinesdimethyldioctadecylammoniumForkhead Transcription FactorsFoxp3 protein, mouseInterferon-gammaQuaternary Ammonium CompoundsRituximabArthritisAutoimmunityB cellsIFN-γTreg cells

Identifiers

PMID25645456
PMCPMC4438566
OpenAlexW1931992866

What OpenQuestion holds

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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.