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Article: LIGHT of pulmonary NKT cells annihilates tissue protective alveolar macrophages in augmenting severe influenza pneumonia

TitleLIGHT of pulmonary NKT cells annihilates tissue protective alveolar macrophages in augmenting severe influenza pneumonia
Authors
KeywordsInfluenza A virus
LIGHT/TNFSF14
Natural killer T cells
Alveolar macrophages
Issue Date2021
PublisherElsevier B.V. and Science China Press. The Journal's web site is located at http://www.sciencedirect.com/science/journal/20959273?sdc=1
Citation
Science Bulletin, 2021, Epub 2021-01-26 How to Cite?
AbstractCD1d-restricted natural killer T (NKT) cells are innate-like T lymphocytes with protective or pathogenic roles in the development of influenza pneumonia. Here, we show that lung-infiltrated and activated NKT cells are the major cellular source of LIGHT/TNFSF14, which determines the severity of pulmonary pneumonia by highly deteriorative influenza A virus (IAV) infection. Compared to wild-type mice, LIGHT−/− mice exhibit much lower morbidity and mortality to IAV, due to alleviated lung damage and reduced apoptosis of alveolar macrophages (AMs). LIGHT preferentially promotes cell death of lymphotoxin β receptors positive (LTβR+) AMs but not herpesvirus entry mediator positive (HVEM+) AMs. Therefore, these results suggest that NKT-derived LIGHT augments cell death of the tissue protective AMs in exacerbating lung pathology and susceptibility to fatal influenza infection. Suppression of LIGHT signaling might be a viable option in the treatment of influenza-associated acute respiratory distress syndrome.
Persistent Identifierhttp://hdl.handle.net/10722/299774
ISSN
2020 Impact Factor: 11.78
2015 SCImago Journal Rankings: 0.477

 

DC FieldValueLanguage
dc.contributor.authorShi, LN-
dc.contributor.authorZhou, Y-
dc.contributor.authorWu, C-
dc.contributor.authorHuang, W-
dc.contributor.authorYuan, F-
dc.contributor.authorChen, J-
dc.contributor.authorWu, Z-
dc.contributor.authorTu, W-
dc.contributor.authorChen, H-
dc.contributor.authorChen, Q-
dc.contributor.authorZhu, M-
dc.contributor.authorPeng, H-
dc.contributor.authorYang, Y-
dc.contributor.authorTang, H-
dc.date.accessioned2021-05-26T03:28:52Z-
dc.date.available2021-05-26T03:28:52Z-
dc.date.issued2021-
dc.identifier.citationScience Bulletin, 2021, Epub 2021-01-26-
dc.identifier.issn2095-9273-
dc.identifier.urihttp://hdl.handle.net/10722/299774-
dc.description.abstractCD1d-restricted natural killer T (NKT) cells are innate-like T lymphocytes with protective or pathogenic roles in the development of influenza pneumonia. Here, we show that lung-infiltrated and activated NKT cells are the major cellular source of LIGHT/TNFSF14, which determines the severity of pulmonary pneumonia by highly deteriorative influenza A virus (IAV) infection. Compared to wild-type mice, LIGHT−/− mice exhibit much lower morbidity and mortality to IAV, due to alleviated lung damage and reduced apoptosis of alveolar macrophages (AMs). LIGHT preferentially promotes cell death of lymphotoxin β receptors positive (LTβR+) AMs but not herpesvirus entry mediator positive (HVEM+) AMs. Therefore, these results suggest that NKT-derived LIGHT augments cell death of the tissue protective AMs in exacerbating lung pathology and susceptibility to fatal influenza infection. Suppression of LIGHT signaling might be a viable option in the treatment of influenza-associated acute respiratory distress syndrome.-
dc.languageeng-
dc.publisherElsevier B.V. and Science China Press. The Journal's web site is located at http://www.sciencedirect.com/science/journal/20959273?sdc=1-
dc.relation.ispartofScience Bulletin-
dc.subjectInfluenza A virus-
dc.subjectLIGHT/TNFSF14-
dc.subjectNatural killer T cells-
dc.subjectAlveolar macrophages-
dc.titleLIGHT of pulmonary NKT cells annihilates tissue protective alveolar macrophages in augmenting severe influenza pneumonia-
dc.typeArticle-
dc.identifier.emailTu, W: wwtu@hku.hk-
dc.identifier.authorityTu, W=rp00416-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.scib.2021.01.026-
dc.identifier.scopuseid_2-s2.0-85102854228-
dc.identifier.hkuros322497-
dc.identifier.volumeEpub 2021-01-26-
dc.publisher.placeUnited States-

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