ArticleEMBO molecular medicine2016
OX40 ligand newly expressed on bronchiolar progenitors mediates influenza infection and further exacerbates pneumonia.
Article in EMBO molecular medicine, 2016. 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, 10 citations in OpenAlex.
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- Supersulphides provide airway protection in viral and chronic lung diseases.Nature communications · 2023Article
- A sesquiterpene isolated from the stems and leaves ofHeliyon · 2022Article
- High serum OX40 ligand correlates with severity and mortality in patients with massive cerebral infarction.Medicine · 2020Article
- Characterization of Influenza A Virus Infection in Mouse Pulmonary Stem/Progenitor Cells.Frontiers in microbiology · 2019Article
- Possible involvement of interleukin-18 in the pathology of hepatobiliary adverse effects related to treatment with ceritinib.BMC cancer · 2018Article
- Peripheral alveolar nitric oxide concentration reflects alveolar inflammation in autoimmune pulmonary alveolar proteinosis.ERJ open research · 2018Article
- OX40 ligand newly expressed on bronchiolar progenitors mediates influenza infection and further exacerbates pneumonia.EMBO molecular medicine · 2016Article
- Beneficial effects of sunitinib on tumor microenvironment and immunotherapy targeting death receptor5.OncoimmunologyArticle
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Influenza virus epidemics potentially cause pneumonia, which is responsible for much of the mortality due to the excessive immune responses. The role of costimulatory OX40-OX40 ligand (OX40L) interactions has been explored in the non-infectious pathology of influenza pneumonia. Here, we describe a critical contribution of OX40L to infectious pathology, with OX40L deficiency, but not OX40 deficiency, resulting in decreased susceptibility to influenza viral infection. Upon infection, bronchiolar progenitors increase in number for repairing the influenza-damaged epithelia. The OX40L expression is induced on the progenitors for the antiviral immunity during the infectious process. However, these defense-like host responses lead to more extensive infection owing to the induced OX40L with α-2,6 sialic acid modification, which augments the interaction with the viral hemagglutinin. In fact, the specific antibody against the sialylated site of OX40L exhibited therapeutic potency in mitigating the OX40L-mediated susceptibility to influenza. Our data illustrate that the influenza-induced expression of OX40L on bronchiolar progenitors has pathogenic value to develop a novel therapeutic approach against influenza.
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