tetano
Editor, Senior Moderator
J Gen Virol. 2011 Dec 14. [Epub ahead of print]
Plasmacytoid dendritic cells and TLR7-dependent signaling promote efficient protection of mice against highly virulent influenza A virus.
Kaminski MM, Ohnemus A, Cornitescu M, Staeheli P.
Source
Virology Freiburg.
Abstract
Type I and type III interferons (IFNs) elicit protective antiviral immune responses during influenza virus infection. Although many cell types can synthesize IFN in response to virus infection, it remains unclear which IFN sources contribute to antiviral protection in vivo. We found that mice carrying functional alleles of the Mx1 influenza virus resistance gene partially lost resistance to infection with a highly pathogenic H7N7 influenza A virus strain if toll-like receptor 7 (TLR7) signaling was compromised. This effect was achieved by deleting either the TLR7 gene or the gene encoding the TLR7 adaptor molecule MyD88. A similar decrease of influenza virus resistance was observed when animals were deprived of plasmacytoid dendritic cells (pDCs) at day 1 post-infection. Our results provide in vivo proof that pDCs contribute to the protection of the lung against influenza A virus infections, presumably via signals from TLR7.
PMID:
22170637
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22170637
Plasmacytoid dendritic cells and TLR7-dependent signaling promote efficient protection of mice against highly virulent influenza A virus.
Kaminski MM, Ohnemus A, Cornitescu M, Staeheli P.
Source
Virology Freiburg.
Abstract
Type I and type III interferons (IFNs) elicit protective antiviral immune responses during influenza virus infection. Although many cell types can synthesize IFN in response to virus infection, it remains unclear which IFN sources contribute to antiviral protection in vivo. We found that mice carrying functional alleles of the Mx1 influenza virus resistance gene partially lost resistance to infection with a highly pathogenic H7N7 influenza A virus strain if toll-like receptor 7 (TLR7) signaling was compromised. This effect was achieved by deleting either the TLR7 gene or the gene encoding the TLR7 adaptor molecule MyD88. A similar decrease of influenza virus resistance was observed when animals were deprived of plasmacytoid dendritic cells (pDCs) at day 1 post-infection. Our results provide in vivo proof that pDCs contribute to the protection of the lung against influenza A virus infections, presumably via signals from TLR7.
PMID:
22170637
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22170637