Plasmacytoid Dendritic Cells Contribute to the Production of IFN-beta via TLR7-MyD88-Dependent Pathway and CTL Priming during Respiratory Syncytial Virus Infection
- 주제(키워드) RSV , plasmacytoid dendritic cell , dendritic cell , type I IFN , cytotoxic CD8(+) T cells
- 주제(기타) Virology
- 등재 SCIE, SCOPUS
- OA유형 Green Submitted, gold, Green Published
- 발행기관 MDPI
- 발행년도 2019
- 총서유형 Journal
- URI http://www.dcollection.net/handler/ewha/000000161463
- 본문언어 영어
- Published As http://dx.doi.org/10.3390/v11080730
- PubMed https://pubmed.ncbi.nlm.nih.gov/31398816
초록/요약
Respiratory syncytial virus (RSV) is the leading cause of respiratory viral infection in infants and children, yet little is known about the antiviral response of plasmacytoid dendritic cells (pDCs) to RSV infection. We tracked the cellular source of interferon-beta using interferon-beta/yellow fluorescent protein (YFP) reporter mice and identified the signaling pathway activated by RSV that induces type I interferon production in pDCs and DCs. Results from in vitro analyses of RSV-stimulated bone marrow cells revealed that RSV induces interferon-beta production in both pDCs and DCs. Kinetic analyses of interferon-beta-producing cells in RSV-infected lung cells in vivo indicated that pDCs are rapidly recruited to sites of inflammation during infection. These cells produced interferon-beta via the TLR7-MyD88-mediated pathway and IFN alpha 1R-mediated pathway rather than the MAVS-mediated pathway. Moreover, pDC-ablated mice exhibited decreased interferon-gamma production and the antigen specificity of CD8(+) T cells. Collectively, these data indicate that pDCs play pivotal roles in cytotoxic T lymphocyte (CTL) responses and are one of producers of type I interferon during RSV infection.
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