Evidence map›Paper›PMID 21949021›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2011

Sensitivity and resistance to regulation by IL-4 during Th17 maturation.

Laura A Cooney, Keara Towery, Judith Endres, David A Fox

Open access · greenAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 2 pooled it
3.2field-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

39 citing papers in PubMed, 2 syntheses or guidelines pooled it, 91 citations in OpenAlex.

  1. The role of IL-17 and Th17 cells in keloid pathogenesis.Archives of dermatological research · 2024
    Pooled it
  2. Pooled it
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  13. Remission of eczema and recovery of Th1 polarization following treatment with Dupilumab in STAT3 hyper IgE syndrome.Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2022
    Article
  14. Review
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  20. Regulation of IL-17A and implications for TGF-β1 comodulation of airway smooth muscle remodeling in severe asthma.American journal of physiology. Lung cellular and molecular physiology · 2019
    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

4 authors at 2 institutions in 2 countries.

Laura A CooneyDivision of Rheumatology, Department of Internal Medicine and Rheumatic Disease Research Core Center, University of Michigan, Ann Arbor, MI 48109, USA.
Keara Towery
Judith Endres
David A Fox
Michigan Medicine · USInstitute for Rheumatic Diseases (Japan) · JP

Funding

Vector CoreP30AR048310 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI TODD, ROBERT F · 2001 to 2010
$5.9M
UNIQUE SURFACE STRUCTURES ON SYNOVIAL CELLSR01AR038477 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FOX, DAVID ALAN · 1991 to 2011
$2.9M
UNIQUE SURFACE STRUCTURES ON RHEUMATOID SYNOVIAL T CELLSR29AR038477 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FOX, DAVID ALAN · 1986 to 1990
–
NIAMS NIH HHS AR38477NIAMS NIH HHS P30 AR048310NIAMS NIH HHS R01 AR038477
6 · The paper itself

Abstract

Th17 cells are highly pathogenic in a variety of immune-mediated diseases, and a thorough understanding of the mechanisms of cytokine-mediated suppression of Th17 cells has great therapeutic potential. In this article, we characterize the regulation of both in vitro- and in vivo-derived Th17 cells by IL-4. We demonstrate that IL-4 suppresses reactivation of committed Th17 cells, even in the presence of TGF-β, IL-6, and IL-23. Downregulation of IL-17 by IL-4 is dependent on STAT6 and mediated by inhibition of STAT3 binding at the Il17a promoter. Although Th1 cytokines were shown to induce IFN-γ expression by Th17 cells, IL-4 does not induce a Th2 phenotype in Th17 cells. Suppression by IL-4 is stable and long-lived when applied to immature Th17 cells, but cells that have undergone multiple rounds of stimulation, either in vivo during a Th17-mediated inflammatory disease, or in vitro, become resistant to suppression by IL-4 and lose the ability to signal through IL-4R. Thus, although IL-4 is a potent suppressor of the Th17 genetic program at early stages after differentiation, prolonged stimulation renders Th17 cells impervious to regulatory cytokines.

Indexed as

AnimalsCell DifferentiationCells, CulturedGATA3 Transcription FactorGrowth InhibitorsImmunophenotypingInterleukin-17Interleukin-4Lymphocyte ActivationMaleMiceMice, Inbred BALB CMice, Inbred C57BLMice, Inbred DBAMice, TransgenicProtein BindingGata3 protein, mouseGATA3 Transcription FactorGrowth InhibitorsInterleukin-17Interleukin-4Stat3 protein, mouseSTAT3 Transcription FactorStat6 protein, mouseSTAT6 Transcription Factor

Identifiers

PMID21949021
PMCPMC3197869
OpenAlexW2099829665

What OpenQuestion holds

Textmetadata
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.