Evidence map›Paper›PMID 31619669›Full record

ArticleNature communications2019

IL-36 promotes anti-viral immunity by boosting sensitivity to IFN-α/β in IRF1 dependent and independent manners.

Peng Wang, Ana M Gamero, Liselotte E Jensen

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.4field-weighted citation impact, top 16% 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

29 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Article
  3. Microbiology spectrum · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Editorial: Viral infection pathogenesis and pathology in nervous system.Frontiers in cellular and infection microbiology · 2025
    Article
  10. Vaccines · 2024
    Article
  11. FloxedCells · 2024
    Article
  12. Article
  13. Article
  14. Article
  15. Serum Interleukin-36 in Pityriasis Rosea: A Potential Biomarker for Disease Severity.The Journal of clinical and aesthetic dermatology · 2023
    Article
  16. Article
  17. Article
  18. Review
  19. Review
  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

3 authors at 1 institution in 1 country.

Peng WangDepartment of Microbiology and Immunology, Temple University Lewis Katz School of Medicine, Philadelphia, PA, 19140, USA.ORCID http://orcid.org/0000-0001-8695-6721
Ana M GameroDepartment of Medical Genetics and Molecular Biochemistry, Temple University Lewis Katz School of Medicine, Philadelphia, PA, 19140, USA.
Liselotte E JensenDepartment of Microbiology and Immunology, Temple University Lewis Katz School of Medicine, Philadelphia, PA, 19140, USA. liselott@temple.edu.ORCID http://orcid.org/0000-0002-0267-8312
Temple University · US

Funding

WORD PROCESSING CENTER--COREP30CA006927 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI Dietmar J Kappes · 1985 to 2026
$138.8M
Interleukin-36 cytokines in antiviral immune responsesR01AI125111 · NIAID · TEMPLE UNIV OF THE COMMONWEALTH · PI JENSEN, LISELOTTE E · 2016 to 2020
$2.0M
NCI NIH HHS P30 CA006927NIAID NIH HHS R01 AI125111
6 · The paper itself

Abstract

The functions of the IL-36 cytokines remain poorly understood. We report a previously unrecognized mechanism whereby IL-36 promotes innate antiviral immunity in mouse and human models of herpes simplex virus-1 (HSV-1) infections. HSV-1 actively suppresses production of type I interferon (IFN); our data reveal that IL-36 overcomes this immune evasion strategy by increasing cellular sensitivity to IFN. IL-36β deficient mice display impaired IFN responses and poorly restrict viral replication in skin keratinocytes. In mouse and human keratinocytes IL-36 elicits an antiviral state driven by STAT1 and STAT2 via enhanced expression of IFNAR1 and IFNAR2 subunits of the type I IFN receptor. The degree of IFN regulatory factor 1 (IRF1) involvement is species dependent, with IRF1 playing a more prominent role in human cells. Similar mechanisms are activated by IL-1. Overall, IL-36 acts as an antiviral cytokine by potentiating type I IFN signaling and thereby upholds immune responses to viruses that limit the production of IFNs.

Indexed as

AnimalsDisease Models, AnimalHerpes SimplexHerpesvirus 1, HumanHumansImmune EvasionInterferon Regulatory Factor-1Interferon Type IInterleukin-1KeratinocytesMiceMice, KnockoutReceptor, Interferon alpha-betaSTAT1 Transcription FactorSTAT2 Transcription FactorUp-RegulationIL-1F8 protein, mouseIL1F9 protein, mouseIL36A protein, humanIL36B protein, humanIL36G protein, humanInterferon Regulatory Factor-1Interferon Type IInterleukin-1interleukin 1F6, mouseReceptor, Interferon alpha-betaSTAT1 Transcription FactorSTAT2 Transcription Factor

Identifiers

PMID31619669
PMCPMC6795910
OpenAlexW2980765413

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.