Evidence map›Paper›PMID 26059829›Full record

ArticleJournal of leukocyte biology2015

Differential effects of IFN-β on IL-12, IL-23, and IL-10 expression in TLR-stimulated dendritic cells.

Jui-Hung Yen, Weimin Kong, Kirsten M Hooper, Frances Emig, Kate M Rahbari, Ping-Chang Kuo, Barbara A Scofield, Doina Ganea

Abstract read
In one paragraph

Article in Journal of leukocyte biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.7field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. IFN-κ Is a Rheostat for Development of Psoriasiform Inflammation.The Journal of investigative dermatology · 2022
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Interferon-β Modulates Inflammatory Response in Cerebral Ischemia.Journal of the American Heart Association · 2016
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Jui-Hung Yen*Department of Microbiology and Immunology, Indiana University School of Medicine, Fort Wayne, Indiana, USA; Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, Pennsylvania, USA.
Weimin Kong*Department of Microbiology and Immunology, Indiana University School of Medicine, Fort Wayne, Indiana, USA; Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, Pennsylvania, USA.
Kirsten M Hooper*Department of Microbiology and Immunology, Indiana University School of Medicine, Fort Wayne, Indiana, USA; Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, Pennsylvania, USA.
Frances Emig*Department of Microbiology and Immunology, Indiana University School of Medicine, Fort Wayne, Indiana, USA; Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, Pennsylvania, USA.
Kate M Rahbari*Department of Microbiology and Immunology, Indiana University School of Medicine, Fort Wayne, Indiana, USA; Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, Pennsylvania, USA.
Ping-Chang Kuo*Department of Microbiology and Immunology, Indiana University School of Medicine, Fort Wayne, Indiana, USA; Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, Pennsylvania, USA.
Barbara A Scofield*Department of Microbiology and Immunology, Indiana University School of Medicine, Fort Wayne, Indiana, USA; Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, Pennsylvania, USA.
Doina Ganea*Department of Microbiology and Immunology, Indiana University School of Medicine, Fort Wayne, Indiana, USA; Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, Pennsylvania, USA dganea@temple.edu.
Temple University · USIndiana University · USIndiana University School of Medicine

Funding

Temple University Minority Access to Research Careers (MARC) programT34GM087239 · NIGMS · TEMPLE UNIV OF THE COMMONWEALTH · PI TANAKA, JACQUELINE C · 2009 to 2018
$5.2M
REGULATION OF IMMUNE CELL APOPTOSIS BY NEUROPEPTIDESR01AI047325 · NIAID · TEMPLE UNIV OF THE COMMONWEALTH · PI GANEA, DOINA · 2001 to 2014
$3.8M
CB2 Receptor Regulatin of Inflammatory Response in EAER01AI084065 · NIAID · TEMPLE UNIV OF THE COMMONWEALTH · PI GANEA, DOINA, TUMA, RONALD F · 2009 to 2012
$1.5M
NIAID NIH HHS R01 AI047325NIAID NIH HHS R01 AI084065NIAID NIH HHS R01AI084065NIAID NIH HHS R01AI47325NIGMS NIH HHS 5T34 GM087239NIGMS NIH HHS T34 GM087239
6 · The paper itself

Abstract

MS is an autoimmune disease characterized by immune cell infiltration in the CNS, leading to cumulative disability. IFN-β, used clinically in RR-MS reduces lesion formation and rates of relapse. Although the molecular mechanisms are not entirely elucidated, myeloid cells appear to be a major target for the therapeutic effects of IFN-β. DCs have a critical role in experimental models of MS through their effect on encephalitogenic Th1/Th17 cell differentiation and expansion. Here we focused on the effects of IFN-β on DC expression of cytokines involved in the control of Th1/Th17 differentiation and expansion. Administration of IFN-β to mice immunized with MOG35-55 inhibited IL-12 and IL-23 expression in splenic DC and reduced in vivo differentiation of Th1/Th17 cells. IFN-β affected cytokine expression in TLR-stimulated DC in a similar manner in vitro, inhibiting IL-12 and IL-23 and stimulating IL-10 at both mRNA and protein levels, by signaling through IFNAR. We investigated the role of the signaling molecules STAT1/STAT2, IRF-1 and IRF-7, and of the PI3K→GSK3 pathway. IFN-β inhibition of the IL-12 subunits p40 and p35 was mediated through STAT1/STAT2, whereas inhibition of IL-23 was STAT1 dependent, and the stimulatory effect on IL-10 expression was mediated through STAT2. IFN-β induces IRF-7 and, to a lesser degree, IRF-1. However, neither IRF mediated the effects of IFN-β on IL-12, IL-23, or IL-10. We found that the PI3K pathway mediated IL-12 inhibition but did not interfere with the inhibition of IL-23 or stimulation of IL-10.

Indexed as

AnimalsDendritic CellsGene Expression RegulationInterferon-betaInterferon Regulatory Factor-1Interferon Regulatory Factor-7Interleukin-10Interleukin-12 Subunit p35Interleukin-12 Subunit p40Interleukin-23MiceMice, KnockoutMyelin-Oligodendrocyte GlycoproteinPeptide FragmentsPhosphatidylinositol 3-KinasesSignal TransductionIL10 protein, mouseIl12a protein, mouseInterferon-betaInterferon Regulatory Factor-1Interferon Regulatory Factor-7Interleukin-10Interleukin-12 Subunit p35Interleukin-12 Subunit p40Interleukin-23Irf1 protein, mouseIrf7 protein, mouseMyelin-Oligodendrocyte Glycoproteinmyelin oligodendrocyte glycoprotein (35-55)Peptide FragmentsPhosphatidylinositol 3-KinasesStat1 protein, mouseSTAT1 Transcription FactorStat3 protein, mouseSTAT3 Transcription FactorToll-Like ReceptorscytokinesIRF1/IRF7PI3K/GSK3STAT1/STAT2Type I interferons

Identifiers

PMID26059829
PMCPMC4600065
OpenAlexW2270700224

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.