ArticleViral immunology2010
Interference with intraepithelial TNF-α signaling inhibits CD8(+) T-cell-mediated lung injury in influenza infection.
Article in Viral immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 23 citations in OpenAlex.
- IL-21 controls CD8Zoological research · 2026Article
- Single-cell dissection of avian (chicken) H1N1 influenza virus coinfection dynamics in mammalian (mouse) and avian (chicken) hosts.Acta biochimica et biophysica Sinica · 2025Article
- Regulation of respiratory CD8+ T-cell immunity by suppressive monocyte-like dendritic cells (MCs).Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- The frequency and function of nucleoprotein-specific CD8Journal of virology · 2024Article
- Mechanisms underlying the therapeutic effects of Gang Huo Qing wen granules in the treatment of influenza based on network pharmacology, molecular docking and molecular dynamics.Scientific reports · 2024Article
- Viral PB1-F2 and host IFN-γ guide ILC2 and T cell activity during influenza virus infection.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Balancing Immune Protection and Immune Pathology by CD8(+) T-Cell Responses to Influenza Infection.Frontiers in immunology · 2016Review
- STAT1 interaction with E3-14.7K in monocytes affects the efficacy of oncolytic adenovirus.Journal of virology · 2014Article
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Corrections and comments
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Authors and funding
8 authors at 6 institutions in 2 countries.
Funding
Abstract
CD8(+) T-cell-mediated pulmonary immunopathology in respiratory virus infection is mediated in large part by antigen-specific TNF-α expression by antiviral effector T cells, which results in epithelial chemokine expression and inflammatory infiltration of the lung. To further define the signaling events leading to lung epithelial chemokine production in response to CD8(+) T-cell antigen recognition, we expressed the adenoviral 14.7K protein, a putative inhibitor of TNF-α signaling, in the distal lung epithelium, and analyzed the functional consequences. Distal airway epithelial expression of 14.7K resulted in a significant reduction in lung injury resulting from severe influenza pneumonia. In vitro analysis demonstrated a significant reduction in the expression of an important mediator of injury, CCL2, in response to CD8(+) T-cell recognition, or to TNF-α. The inhibitory effect of 14.7K on CCL2 expression resulted from attenuation of NF-κB activity, which was independent of Iκ-Bα degradation or nuclear translocation of the p65 subunit. Furthermore, epithelial 14.7K expression inhibited serine phosphorylation of Akt, GSK-3β, and the p65 subunit of NF-κB, as well as recruitment of NF-κB for DNA binding in vivo. These results provide insight into the mechanism of 14.7K inhibition of NF-κB activity, as well as further elucidate the mechanisms involved in the induction of T-cell-mediated immunopathology in respiratory virus infection.
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Registered trials
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.