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European Journal of Immunology
Article . 2004 . Peer-reviewed
License: Wiley Online Library User Agreement
Data sources: Crossref
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Dendritic cells respond to influenza virus through TLR7‐ and PKR‐independent pathways

Authors: Andrzej Dzionek; Jens Fischer; Marina Cella; Marco Colonna; Andrew Pekosz; Celeste M. Newby; Winfried Barchet; +1 Authors

Dendritic cells respond to influenza virus through TLR7‐ and PKR‐independent pathways

Abstract

AbstractNatural interferon‐producing cells (IPC) secrete type I IFN (IFN‐α and ‐β) in response to influenza virus. This process is independent of viral replication and is mediated by Toll‐like receptor 7 (TLR7), which recognizes single‐stranded RNA (ssRNA). DC also express TLR7 but its function in DC response to influenza virus is unknown. To address this, we compared the DC and IPC responses to influenza virus and ssRNA oligoribonucleotides (ORN) that activate TLR7. When stimulated by ORN in vitro and in vivo, DC matured and produced inflammatory cytokines but not IFN‐α. DC did secrete IFN‐α in response to influenza virus. However, this response was independent of TLR7 signaling and required viral replication but not dsRNA‐activated protein kinase (PKR). We conclude that DC and IPC are hard‐wired to secrete IFN‐α via different pathways, reflecting their complementary but distinct roles in anti‐viral immunity.

Keywords

Mice, Knockout, Membrane Glycoproteins, Oligoribonucleotides, Base Sequence, Interferon-alpha, Receptors, Cell Surface, Dendritic Cells, In Vitro Techniques, Viral Nonstructural Proteins, Antigens, Differentiation, Immunity, Innate, Mice, Inbred C57BL, Mice, Toll-Like Receptor 7, Influenza A virus, Myeloid Differentiation Factor 88, Animals, Cytokines, Receptors, Immunologic, Adaptor Proteins, Signal Transducing

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citations
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
107
Top 10%
Top 10%
Top 1%
bronze