Evidence map›Paper›PMID 26441347›Full record

ArticleScientific reports2015

IL-1β promotes Th17 differentiation by inducing alternative splicing of FOXP3.

Reiner K W Mailer, Anne-Laure Joly, Sang Liu, Szabolcs Elias, Jesper Tegner, John Andersson

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 5% 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

86 citing papers in PubMed, 1 synthesis or guideline pooled it, 126 citations in OpenAlex.

  1. Pooled it
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  4. Immune Checkpoint Inhibitor-Associated Inflammatory Arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2026
    Review
  5. Article
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  7. Article
  8. Article
  9. Review
  10. Immune-responsive gene 1: The mitochondrial key to Th17 cell pathogenicity in CNS autoimmunity.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Differential induction of donor-reactive Foxp3American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2024
    Article
  19. Get Spliced: Uniting Alternative Splicing and Arthritis.International journal of molecular sciences · 2024
    Review
  20. Article

26 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

6 authors at 1 institution in 1 country.

Reiner K W MailerTranslational Immunology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
Anne-Laure JolyTranslational Immunology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
Sang LiuTranslational Immunology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
Szabolcs EliasUnit of Computational Medicine, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
Jesper TegnerUnit of Computational Medicine, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
John AnderssonTranslational Immunology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
Karolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD4(+)FOXP3(+) regulatory T (Treg) cells are essential for maintaining immunological self-tolerance. Treg cell development and function depend on the transcription factor FOXP3, which is present in several distinct isoforms due to alternative splicing. Despite the importance of FOXP3 in the proper maintenance of Treg cells, the regulation and functional consequences of FOXP3 isoform expression remains poorly understood. Here, we show that in human Treg cells IL-1β promotes excision of FOXP3 exon 7. FOXP3 is not only expressed by Treg cells but is also transiently expressed when naïve T cells differentiate into Th17 cells. Forced splicing of FOXP3 into FOXP3Δ2Δ7 strongly favored Th17 differentiation in vitro. We also found that patients with Crohn's disease express increased levels of FOXP3 transcripts lacking exon 7, which correlate with disease severity and IL-17 production. Our results demonstrate that alternative splicing of FOXP3 modulates T cell differentiation. These results highlight the importance of characterizing FOXP3 expression on an isoform basis and suggest that immune responses may be manipulated by modulating the expression of FOXP3 isoforms, which has broad implications for the treatment of autoimmune diseases.

Indexed as

Alternative SplicingCell DifferentiationBlotting, WesternCells, CulturedCrohn DiseaseForkhead Transcription FactorsHumansImmune ToleranceInterleukin-17Interleukin-1betaLymphocyte ActivationPromoter Regions, GeneticProtein IsoformsReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionRNA, MessengerForkhead Transcription FactorsFOXP3 protein, humanInterleukin-17Interleukin-1betaProtein IsoformsRNA, Messenger

Identifiers

PMID26441347
PMCPMC4593960
OpenAlexW2413233050

What OpenQuestion holds

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LicenceCC BY
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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.