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https://doi.org/10.15252/embj.201899176
Title: | Loss of T-bet confers survival advantage to influenza-bacterial superinfection | Authors: | Er, Jun Zhi Koean, Ricky Abdi Gunawan Ding, Jeak Ling |
Keywords: | Science & Technology Life Sciences & Biomedicine Biochemistry & Molecular Biology Cell Biology bacteria influenza Streptococcus pneumonia T-bet IFN-GAMMA PRODUCTION ACUTE EOSINOPHILIC PNEUMONIA A VIRUS-INFECTION PANDEMIC INFLUENZA CUTTING EDGE TH17 CELLS INCREASED SUSCEPTIBILITY ALVEOLAR MACROPHAGES ALLOGRAFT-REJECTION INTERFERON-GAMMA |
Issue Date: | 3-Jan-2019 | Publisher: | WILEY | Citation: | Er, Jun Zhi, Koean, Ricky Abdi Gunawan, Ding, Jeak Ling (2019-01-03). Loss of T-bet confers survival advantage to influenza-bacterial superinfection. EMBO JOURNAL 38 (1). ScholarBank@NUS Repository. https://doi.org/10.15252/embj.201899176 | Abstract: | The transcription factor, T-bet, regulates type 1 inflammatory responses against a range of infections. Here, we demonstrate a previously unaddressed role of T-bet, to influenza virus and bacterial superinfection. Interestingly, we found that T-bet deficiency did not adversely affect the efficacy of viral clearance or recovery compared to wild-type hosts. Instead, increased infiltration of neutrophils and production of Th17 cytokines (IL-17 and IL-22), in lungs of influenza virus-infected T-bet −/− mice, were correlated with survival advantage against subsequent infection by Streptococcus pneumoniae. Neutralization of IL-17, but not IL-22, in T-bet −/− mice increased pulmonary bacterial load, concomitant with decreased neutrophil infiltration and reduced survival of T-bet −/− mice. IL-17 production by CD8 + , CD4 + and γδ T cell types was identified to contribute to this protection against bacterial superinfection. We further showed that neutrophil depletion in T-bet −/− lungs increased pulmonary bacterial burden. These results thus indicate that despite the loss of T-bet, immune defences required for influenza viral clearance are fully functional, which in turn enhances protective type 17 immune responses against lethal bacterial superinfections. | Source Title: | EMBO JOURNAL | URI: | https://scholarbank.nus.edu.sg/handle/10635/193722 | ISSN: | 02614189 14602075 |
DOI: | 10.15252/embj.201899176 |
Appears in Collections: | Staff Publications Elements |
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