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Special Issue: Applications of CRISPR Technology in Virology 2018
Open AccessArticle

Exogenous Interleukin-33 Contributes to Protective Immunity via Cytotoxic T-Cell Priming against Mucosal Influenza Viral Infection

by 1,†, 1,†, 1, 2 and 1,2,3,*
1
Biomedical Science and Engineering Interdisciplinary Program, Korea Advanced Institute of Science and Technology (KAIST), Daejeon 34141, Korea
2
Graduate School of Medical Science and Engineering, KAIST, Daejeon 34141, Korea
3
KAIST Institute for Health Science and Technology, KAIST, Daejeon 34141, Korea
*
Author to whom correspondence should be addressed.
These authors contributed equally to the work.
Viruses 2019, 11(9), 840; https://doi.org/10.3390/v11090840
Received: 10 June 2019 / Revised: 21 August 2019 / Accepted: 8 September 2019 / Published: 10 September 2019
(This article belongs to the Section Animal Viruses)
Influenza is an infectious respiratory illness caused by the influenza virus. Though vaccines against influenza exist, they have limited efficacy. To additionally develop effective treatments, there is a need to study the mechanisms of host defenses from influenza viral infections. To date, the mechanism by which interleukin (IL)-33 modulates the antiviral immune response post-influenza infection is unclear. In this study, we demonstrate that exogenous IL-33 enhanced antiviral protection against influenza virus infection. Exogenous IL-33 induced the recruitment of dendritic cells, increased the secretion of pro-inflammatory cytokine IL-12, and promoted cytotoxic T-cell responses in the local microenvironment. Thus, our findings suggest a role of exogenous IL-33 in the antiviral immune response against influenza infection. View Full-Text
Keywords: IL-33; influenza virus; antiviral immunity IL-33; influenza virus; antiviral immunity
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MDPI and ACS Style

Kim, C.W.; Yoo, H.J.; Park, J.H.; Oh, J.E.; Lee, H.K. Exogenous Interleukin-33 Contributes to Protective Immunity via Cytotoxic T-Cell Priming against Mucosal Influenza Viral Infection. Viruses 2019, 11, 840.

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