Evidence map›Paper›PMID 23455508›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2013

Independent and interdependent immunoregulatory effects of IL-27, IFN-β, and IL-10 in the suppression of human Th17 cells and murine experimental autoimmune encephalomyelitis.

Denise C Fitzgerald, Zoë Fonseca-Kelly, Melissa L Cullimore, Pegah Safabakhsh, Christiaan J M Saris, Guang-Xian Zhang, Abdolmohamad Rostami

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.1field-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

30 citing papers in PubMed, 47 citations in OpenAlex.

  1. Characterization of an isogenicInfection and immunity · 2026
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  16. Treg-specific IL-27Rα deletion uncovers a key role for IL-27 in Treg function to control autoimmunity.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  17. Article
  18. Article
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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

7 authors at 4 institutions in 2 countries.

Denise C FitzgeraldCentre for Infection and Immunity, Queen's University Belfast, Belfast BT9 7AE, Northern Ireland, United Kingdom. d.fitzgerald@qub.ac.uk
Zoë Fonseca-Kelly
Melissa L Cullimore
Pegah Safabakhsh
Christiaan J M Saris
Guang-Xian Zhang
Abdolmohamad Rostami
Thomas Jefferson University · USAmgen (United States) · USMassachusetts Eye and Ear Infirmary · USQueen's University Belfast · GB

Funding

Regulation of Immunity and Autoreactivity by the Mer Receptor Kinase SubfamilyU19AI082726 · NIAID · THOMAS JEFFERSON UNIVERSITY · PI ROSTAMI, A.M. · 2009 to 2013
$2.9M
The Role of the TH17 cells in the pathogenesis of EAER01NS046782 · NINDS · THOMAS JEFFERSON UNIVERSITY · PI ROSTAMI, A.M. · 2003 to 2013
$2.7M
Biotechnology and Biological Sciences Research Council BB/J01026X/1NIAID NIH HHS U19 AI082726NINDS NIH HHS 2R01NS046782NINDS NIH HHS R01 NS046782PHS HHS 1U19A1082726
6 · The paper itself

Abstract

IFN-β, IL-27, and IL-10 have been shown to exert a range of similar immunoregulatory effects in murine and human experimental systems, particularly in Th1- and Th17-mediated models of autoimmune inflammatory disease. In this study we sought to translate some of our previous findings in murine systems to human in vitro models and delineate the interdependence of these different cytokines in their immunoregulatory effects. We demonstrate that human IL-27 upregulates IL-10 in T cell-activated PBMC cultures and that IFN-β drives IL-27 production in activated monocytes. IFN-β-driven IL-27 is responsible for the upregulation of IL-10, but not IL-17 suppression, by IFN-β in human PBMCs. Surprisingly, IL-10 is not required for the suppression of IL-17 by either IL-27 or IFN-β in this model or in de novo differentiating Th17 cells, nor is IL-27 signaling required for the suppression of experimental autoimmune encephalomyelitis (EAE) by IFN-β in vivo. Furthermore, and even more surprisingly, IL-10 is not required for the suppression of Th17-biased EAE by IL-27, in sharp contrast to Th1-biased EAE. In conclusion, IFN-β and IL-27 both induce human IL-10, both suppress human Th17 responses, and both suppress murine EAE. However, IL-27 signaling is not required for the therapeutic effect of IFN-β in EAE. Suppression of Th17-biased EAE by IL-27 is IL-10-independent, in contrast to its mechanism of action in Th1-biased EAE. Taken together, these findings delineate a complex set of interdependent and independent immunoregulatory mechanisms of IFN-β, IL-27, and IL-10 in human experimental models and in murine Th1- and Th17-driven autoimmunity.

Indexed as

AnimalsAutoimmunityCell DifferentiationEncephalomyelitis, Autoimmune, ExperimentalFemaleHumansImmunologic FactorsInterferon-betaInterleukin-10InterleukinsMiceMonocytesTh17 CellsT-Lymphocyte SubsetsImmunologic FactorsInterferon-betaInterleukin-10InterleukinsMYDGF protein, human

Identifiers

PMID23455508
PMCPMC5027611
OpenAlexW2130776527

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.