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Cited 2 time in webofscience Cited 3 time in scopus
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Monocytes Contribute to IFN-beta Production via the MyD88-Dependent Pathway and Cytotoxic T-Cell Responses against Mucosal Respiratory Syncytial. Virus Infectionopen access

Authors
Kim, Tae HoonKim, Chae WonOh, Dong SunJung, Hi EunLee, Heung Kyu
Issue Date
Aug-2021
Publisher
KOREA ASSOC IMMUNOLOGISTS
Keywords
Respiratory syncytial virus; Type I interferon; Interferon beta; Monocyte
Citation
IMMUNE NETWORK, v.21, no.4
Indexed
SCIE
SCOPUS
KCI
Journal Title
IMMUNE NETWORK
Volume
21
Number
4
URI
https://scholarworks.bwise.kr/gnu/handle/sw.gnu/3417
DOI
10.4110/in.2021.21.e27
ISSN
1598-2629
Abstract
Respiratory syncytial virus (RSV) is the leading cause of respiratory viral infection in infants and children. However, little is known about the contribution of monocytes to antiviral responses against RSV infection. We identified the IFN-beta production of monocytes using IFN-beta/YFP reporter mice. The kinetic analysis of IFN-beta-producing cells in in vivo RSV-infected lung cells indicated that monocytes are recruited to the inflamed lung during the early phase ofinfection. These cells produced IFN-beta via the myeloid differentiation factor 88-mediated pathway, rather than the TLR7- or mitochondrial antiviral signaling protein-mediated pathway. In addition, monocyte-ablated mice exhibited decreased numbers of IFN-gamma-producing and RSV Ag-specific CD8(+) T cells. Collectively, these data indicate that monocytes play pivotal roles in cytotoxic T-cell responses and act as type HFN producers during RSV infection.
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