Evidence map›Paper›PMID 24890725›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2014

IL-27 limits central nervous system viral clearance by promoting IL-10 and enhances demyelination.

Maria Teresa P de Aquino, Parul Kapil, David R Hinton, Timothy W Phares, Shweta S Puntambekar, Carine Savarin, Cornelia C Bergmann, Stephen A Stohlman

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

31 citing papers in PubMed, 42 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Role of IL-27 in HSV-1-Induced Herpetic Stromal Keratitis.Journal of immunology (Baltimore, Md. : 1950) · 2023
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
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  15. Review
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  17. Review
  18. Article
  19. IL-27 promotes the expansion of self-renewing CD8The Journal of experimental medicine · 2019
    Article
  20. 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

8 authors at 2 institutions in 1 country.

Maria Teresa P de AquinoDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195; and.
Parul KapilDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195; and.
David R HintonDepartment of Pathology, University of Southern California Keck School of Medicine, Los Angeles, CA 90089.
Timothy W PharesDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195; and.
Shweta S PuntambekarDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195; and.
Carine SavarinDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195; and.
Cornelia C BergmannDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195; and.
Stephen A StohlmanDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195; and stohlms2@ccf.org.
Cleveland Clinic · USUniversity of Southern California · US

Funding

T Cell Dependent Regulation of Viral PersistenceP01NS064932 · NINDS · CLEVELAND CLINIC LERNER COM-CWRU · PI BERGMANN, CORNELIA · 2009 to 2013
$7.9M
NINDS NIH HHS NS064932NINDS NIH HHS P01 NS064932
6 · The paper itself

Abstract

IL-27 is a pleiotropic member of the IL-6 and IL-12 cytokine family composed of the IL-27p28 and the EBV-induced gene 3. IL-27 and its receptor mRNA are both upregulated in the CNS during acute encephalomyelitis induced by the JHM strain of mouse hepatitis virus (JHMV) and sustained during viral persistence. Contributions of IL-27 to viral pathogenesis were evaluated by infection of IL-27Rα-chain-deficient (IL-27Rα(-/-)) mice. The absence of IL-27 signaling accelerated virus control within the CNS associated with increased IFN-γ secreting virus-specific CD4+ and CD8+ T cells. Abrogation of IL-27 signaling did not affect virus-specific CD8+ T cell-mediated IL-10 production or cytolytic activity or Foxp3+ regulatory T cell populations. However, IL-10 production by virus-specific CD4+ T cells was reduced significantly. Despite increased T cell-mediated antiviral function in IL-27Rα(-/-) mice, the virus persisted in the CNS at similar levels as in wild-type mice. Nevertheless, IL-27Rα(-/-) mice exhibited decreased clinical disease during persistence, coincident with less severe demyelination, the hallmark tissue damage associated with JHMV infection. Overall, these data demonstrate that in contrast to viral infections at other sites, IL-27 does not play a proinflammatory role during JHMV-induced encephalomyelitis. Rather, it limits CNS inflammation and impairs control of CNS virus replication via induction of IL-10 in virus-specific CD4+ T cells. Furthermore, in contrast to its protective role in limiting CNS autoimmunity and preventing immunopathology, these data define a detrimental role of IL-27 in promoting demyelination by delaying viral control.

Indexed as

AnimalsCentral Nervous SystemCoronavirus InfectionsDemyelinating DiseasesEncephalomyelitis, Acute DisseminatedInterleukin-10InterleukinsMiceMice, KnockoutMurine hepatitis virusSignal TransductionT-Lymphocytes, RegulatoryIL10 protein, mouseIl27 protein, mouseInterleukin-10Interleukins

Identifiers

PMID24890725
PMCPMC4067872
OpenAlexW2109675984

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.