Evidence map›Paper›PMID 22359619›Full record

ArticlePloS one2012

Hemagglutinin from the H5N1 virus activates Janus kinase 3 to dysregulate innate immunity.

Wei Xu, Minhui Chen, Nanhai Ge, Jun Xu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 18% 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, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Mechanisms of cardiovascular toxicity induced by PMEnvironmental science and pollution research international · 2021
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. TACE in perinatal mouse lung epithelial cells promotes lung saccular formation.American journal of physiology. Lung cellular and molecular physiology · 2013
    Article
  13. Review
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

4 authors at 2 institutions in 1 country.

Wei XuState Key Laboratory of Respiratory Disease, Guangzhou Institute of Respiratory Diseases, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, People's Republic of China.
Minhui Chen
Nanhai Ge
Jun Xu
First Affiliated Hospital of Guangzhou Medical University · CNState Key Laboratory of Respiratory Disease · CN

Funding

Southern HIV and Alcohol Research Consortium Administrative and Research Support CoreU24AA022002 · NIAAA · UNIVERSITY OF FLORIDA · PI COOK, ROBERT L · 2012 to 2022
$5.5M
NIAAA NIH HHS U24 AA022002
6 · The paper itself

Abstract

Highly pathogenic avian influenza viruses (HPAIVs) cause severe disease in humans. There are no effective vaccines or antiviral therapies currently available to control fatal outbreaks due in part to the lack of understanding of virus-mediated immunopathology. In our study, we used hemagglutinin (HA) of H5N1 virus to investigate the related signaling pathways and their relationship to dysregulated innate immune reaction. We found the HA of H5N1 avian influenza triggered an abnormal innate immune signalling in the pulmonary epithelial cells, through an unusual process involving activation of Janus kinase 3 (JAK3) that is exclusively associated with γc chain and is essential for signaling via all γc cytokine receptors. By using a selective JAK3 inhibitor and JAK3 knockout mice, we have, for the first time, demonstrated the ability to target active JAK3 to counteract injury to the lungs and protect immunocytes from acute hypercytokinemia -induced destruction following the challenge of H5N1 HA in vitro and in vivo. On the basis of the present data, it appears that the efficacy of selective JAK3 inhibition is likely based on its ability to block multiple cytokines and protect against a superinflammatory response to pathogen-associated molecular patterns (PAMPs) attack. Our findings highlight the potential value of selective JAK3 inhibitor in treating the fatal immunopathology caused by H5N1 challenge.

Indexed as

AnimalsCytokinesEpithelial CellsHemagglutininsImmunity, InnateInfluenza A Virus, H5N1 SubtypeJanus Kinase 3LungMiceMice, KnockoutSignal TransductionCytokinesHemagglutininsJak3 protein, mouseJanus Kinase 3

Identifiers

PMID22359619
PMCPMC3280993
OpenAlexW2100081206

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.