Er JZ, Koean RAG, Ding JL. Loss of T-bet confers survival advantage to influenza-bacterial superinfection. EMBO J. 2018 Oct 15.
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.
See Also:
Latest articles in those days:
- Cross-species spill-over potential of the H9N2 bat influenza A virus 9 hours ago
- Bat-borne H9N2 influenza virus evades MxA restriction and exhibits efficient replication and transmission in ferrets 9 hours ago
- Epidemiological characteristics of human infections with avian influenza A(H5N6) virus, China and Laos: A multiple case descriptive analysis, February 2014-June 2023 1 days ago
- Interim Estimates of 2023-2024 Seasonal Influenza Vaccine Effectiveness Among Adults in Korea 1 days ago
- Abundant Intra-Subtype Reassortment Revealed in H13N8 Influenza Viruses 2 days ago
[Go Top] [Close Window]