Evidence map›Paper›PMID 34983110›Full record

ArticleAllergy, asthma & immunology research2022

OASL1-Mediated Inhibition of Type I IFN Reduces Influenza A Infection-Induced Airway Inflammation by Regulating ILC2s.

Yuna Chang, Ji-Seon Kang, Keehoon Jung, Doo Hyun Chung, Sang-Jun Ha, Young-Joon Kim, Hye Young Kim

Open access · diamondAbstract read
In one paragraph

Article in Allergy, asthma & immunology research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 27% 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

13 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. The role of innate immune system in respiratory viral infection related asthma.Frontiers in cellular and infection microbiology · 2025
    Review
  9. Interleukin-1 signaling and CD4Frontiers in immunology · 2025
    Article
  10. Article
  11. Article
  12. Review
  13. 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

7 authors at 2 institutions in 2 countries.

Yuna ChangLaboratory of Mucosal Immunology, Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Korea.ORCID https://orcid.org/0000-0002-4068-3171
Ji-Seon KangGenome Research Center, Department of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, Korea.ORCID https://orcid.org/0000-0003-1830-7329
Keehoon JungDepartment of Biomedical Sciences, BK21 Plus Biomedical Science Project, Seoul National University College of Medicine, Seoul, Korea.ORCID https://orcid.org/0000-0002-2199-5292
Doo Hyun ChungDepartment of Pathology, Seoul National University College of Medicine, Seoul, Korea.ORCID https://orcid.org/0000-0002-9948-8485
Sang-Jun HaSystem Immunology Laboratory, Department of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, Korea.ORCID https://orcid.org/0000-0002-1192-6031
Young-Joon KimGenome Research Center, Department of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, Korea.ORCID https://orcid.org/0000-0001-5061-587X
Hye Young KimLaboratory of Mucosal Immunology, Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Korea.ORCID https://orcid.org/0000-0001-5978-512X
Seoul National University · KRYonsei University · KR

Funding

National Research Foundation of Korea NRF-2019R1A2C2087574National Research Foundation of Korea SRC 2017R1A5A1014560
6 · The paper itself

Abstract

purposeThree observations drove this study. First, 2'-5'-oligoadenylate synthetase-like protein (OASL) is a negative regulator of type I interferon (IFN). Second, type I IFN plays a central role during virus infections and the pathogenesis of various diseases, including asthma. Third, influenza A virus (IAV) causes non-eosinophilic asthma. To evaluate the potential relationships between OASL, type I IFN, and pulmonary innate immune cells in IAV-induced acute airway inflammation by using

methodsAsthma was induced in wild-type (WT) and

resultsIn the IAV-induced asthma model,

conclusionsOASL1 may impede the IAV-induced acute airway inflammation that drives AHR by inhibiting IAV-induced type I IFN production from lung DCs, thereby preserving the functions of lung ILC2s, including their amphiregulin production.

Indexed as

airway hyperreactivityamphiregulindendritic cellinfluenza A viruslungmiceOligoadenylate synthetase-like proteintype 2 innate lymphoid cellstype I interferon

Identifiers

PMID34983110
PMCPMC8724833
OpenAlexW4205468938

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.