Plasmacytoid Dendritic Cells Limit Viral Replication, Pulmonary Inflammation, and Airway Hyperresponsiveness in Respiratory Syncytial Virus Infection
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Plasmacytoid dendritic cells (pDC), as major producers of IFN-α, are thought not only to be pivotal in antiviral immunity, but also to limit allergic inflammation. In this study, we delineate the role of pDC in a mouse model of respiratory syncytial virus (RSV)-induced airway inflammation. Bone marrow-derived pDC generated high levels of IFN-α upon RSV infection, and the percentage of pDC expressing MHC class II and maturation-associated costimulatory molecules was increased. However, their weak Ag-presenting capacity was not enhanced. Furthermore, pDC induced marked levels of IL-10 in T cell cultures irrespective of infection. In vivo, numbers of pDC in the lung increased early after RSV infection and remained elevated throughout the inflammatory phase and the resolution phase of infection. Depletion of pDC resulted in increases in peak RSV titers, pulmonary inflammation, and airway hyperresponsiveness. In contrast, adoptive transfer of activated pDC to the airways reduced RSV copy numbers. In conclusion, RSV infection induces activation of murine pDC with robust IFN-α production, limiting replication and accelerating elimination of RSV. In addition to this innate response, pDC also may play an immune regulatory role in reducing pulmonary inflammation and inhibiting the development of airway hyperresponsiveness.
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Rhinoviruses have been shown to be major regulators of airway remodeling processes, involving not only the airway epithelium but also other components of the airway mucosa.
“Rhinoviruses have been shown to be major regulators of such airway remodeling processes, involving not only the airway epithelium but also other components of the airway mucosa.”
From The airway epithelium: soldier in the fight against respiratory viruses (2011) · cites this paper as [303]
Rhinoviruses may lead to subepithelial fibrosis by the induction of TGF-β, MMP-9, and MMP-10 production, resulting in enhanced degradation and abnormal repair of the extracellular matrix.
“In addition, they may lead to subepithelial fibrosis by the induction of TGF-β, MMP-9, and MMP-10 production, resulting in enhanced degradation and abnormal repair of the extracellular matrix (26, 303).”
From The airway epithelium: soldier in the fight against respiratory viruses (2011) · cites this paper as [303]
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- Authors
- Wang, H., Peters, N., & Schwarze, J.
- Affiliations
- Imperial College London (GB)
- Department of Respiratory Medicine, National Heart and Lung Institute and Wright Fleming Institute of Infection and Immunity, Imperial College London , London ,
- ORCID
- Wang, Hongwei
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2006-11-01
- Volume
- 177
- Issue
- 9
- Pages
- 6263-6270
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1661249704
- Cited by
- 149
- References
- 42
- Citations by year
- 2025: 3 · 2024: 4 · 2023: 4 · 2022: 5 · 2021: 2 · 2020: 8 · 2019: 2 · 2018: 5 · 2017: 12 · 2016: 4 · 2015: 10 · 2014: 7 · 2013: 11 · 2012: 9
- FWCI
- 9.48
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Amgen
- Wellcome Trust (067454)
- Topics
- Health Sciences › Medicine › Epidemiology › Respiratory viral infections research
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Keywords
- plasmacytoid dendritic cells, respiratory syncytial virus, interferon-alpha, airway hyperresponsiveness, lung inflammation, viral replication, IL-10, dendritic cell maturation, MHC class II, antigen presentation, pDC depletion, adoptive transfer, innate immunity, immune regulation
- MeSH terms
- Animals, Dendritic Cells, Humans, Pneumonia, Viral, T-Lymphocytes, Virus Replication, Interferon-alpha, Respiratory Syncytial Virus, Human, Respiratory Syncytial Virus Infections, CD11c Antigen, Cell Proliferation, Mice
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