Evidence map›Paper›PMID 25275588›Full record

ArticleCell death & disease2014

Severe influenza A(H1N1)pdm09 infection induces thymic atrophy through activating innate CD8(+)CD44(hi) T cells by upregulating IFN-γ.

B Liu, X Zhang, W Deng, J Liu, H Li, M Wen, L Bao, J Qu, Y Liu, F Li and 4 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in Cell death & disease, 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
1.5field-weighted citation impact, top 19% 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, 50 citations in OpenAlex.

  1. Article
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  4. Review
  5. Article
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  8. Development of a humanized HLA-A30 transgenic mouse model.Animal models and experimental medicine · 2022
    Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Recirculating IL-1R2Cellular & molecular immunology · 2021
    Article
  15. Infection-Associated Thymic Atrophy.Frontiers in immunology · 2021
    Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. 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

14 authors at 5 institutions in 1 country.

B LiuDepartment of Infectious Diseases and Clinical Microbiology, Beijing Chao-Yang Hospital, Beijing Institute of Respiratory Medicine, Capital Medical University, Beijing, China.
X ZhangDepartment of Immunology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
W DengInstitute of Laboratory Animal Sciences, Chinese Academy of Medical Sciences, Beijing, China.
J LiuNational Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention (China CDC), Beijing, China.
H LiDepartment of Infectious Diseases and Clinical Microbiology, Beijing Chao-Yang Hospital, Beijing Institute of Respiratory Medicine, Capital Medical University, Beijing, China.
M WenDepartment of Immunology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
L BaoInstitute of Laboratory Animal Sciences, Chinese Academy of Medical Sciences, Beijing, China.
J QuDepartment of Infectious Diseases and Clinical Microbiology, Beijing Chao-Yang Hospital, Beijing Institute of Respiratory Medicine, Capital Medical University, Beijing, China.
Y LiuDepartment of Infectious Diseases and Clinical Microbiology, Beijing Chao-Yang Hospital, Beijing Institute of Respiratory Medicine, Capital Medical University, Beijing, China.
F LiInstitute of Laboratory Animal Sciences, Chinese Academy of Medical Sciences, Beijing, China.
Y AnDepartment of Immunology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
C QinInstitute of Laboratory Animal Sciences, Chinese Academy of Medical Sciences, Beijing, China.
B CaoDepartment of Infectious Diseases and Clinical Microbiology, Beijing Chao-Yang Hospital, Beijing Institute of Respiratory Medicine, Capital Medical University, Beijing, China.
C Wang1] Department of Infectious Diseases and Clinical Microbiology, Beijing Chao-Yang Hospital, Beijing Institute of Respiratory Medicine, Capital Medical University, Beijing, China [2] Department of Respiratory Medicine, Capital Medical University, Beijing, China [3] Beijing Institute of Respiratory Medicine, Beijing Key Laboratory of Respiratory and Pulmonary Circulation Disorders, Beijing, China [4] Beijing Institute of Respiratory Medicine, Beijing Hospital, Ministry of Heath, P. R. China, Beijing, China.
Capital Medical University · CNBeijing Chao-Yang Hospital · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNChinese Center For Disease Control and Prevention · CNInstitute of Laboratory Animal Science · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thymic atrophy has been described as a consequence of infection by several pathogens including highly pathogenic avian influenza virus and is induced through diverse mechanisms. However, whether influenza A(H1N1)pdm09 infection induces thymic atrophy and the mechanisms underlying this process have not been completely elucidated. Our results show that severe infection of influenza A(H1N1)pdm09 led to progressive thymic atrophy and CD4+ CD8+ double-positive (DP) T-cells depletion due to apoptosis. The viruses were present in thymus, where they activated thymic innate CD8(+)CD44(hi) single-positive (SP) thymocytes to secrete a large amount of IFN-γ. Milder thymic atrophy was observed in innate CD8+ T-cell-deficient mice (C57BL/6J). Neutralization of IFN-γ could significantly rescue the atrophy, but peramivir treatment did not significantly alleviate thymic atrophy. In this study, we demonstrated that thymic innate CD8(+)CD44(hi) SP T-cells have critical roles in influenza A(H1N1)pdm09 infection-induced thymic atrophy through secreting IFN-γ. This exceptional mechanism might serve as a target for the prevention and treatment of thymic atrophy induced by influenza A(H1N1)pdm09.

Indexed as

Immunity, InnateAnimalsAntibodies, MonoclonalAntiviral AgentsAtrophyCD8-Positive T-LymphocytesDisease Models, AnimalFemaleHost-Pathogen InteractionsHyaluronan ReceptorsInfluenza A Virus, H1N1 SubtypeInterferon-gammaLymphocyte ActivationMice, Inbred BALB CMice, Inbred C57BLOrthomyxoviridae InfectionsAntibodies, MonoclonalAntiviral AgentsCd44 protein, mouseHyaluronan ReceptorsInterferon-gamma

Identifiers

PMID25275588
PMCPMC4649502
OpenAlexW2045123063

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.