Language:

Plasmacytoid dendritic cells promote host defense against acute pneumovirus infection via the TLR7-MyD88-dependent signaling pathway

The Journal of immunology (1950), 2011-05, Vol.186 (10), p.5938-5948 [Peer Reviewed Journal]

ISSN: 0022-1767 ;EISSN: 1550-6606 ;DOI: 10.4049/jimmunol.1002635 ;PMID: 21482736

Full text available

Citations Cited by

Actions
1. Add to My Research
2. Remove from My Research
3. E-mail
4. Print
5. Permalink
6. Citation
7. EasyBib
8. EndNote
9. RefWorks
10. Delicious
11. Export RIS
12. Export BibTeX

Title:
Plasmacytoid dendritic cells promote host defense against acute pneumovirus infection via the TLR7-MyD88-dependent signaling pathway
Author: Davidson, Sophia ; Kaiko, Gerard ; Loh, Zhixuan ; Lalwani, Amit ; Zhang, Vivian ; Spann, Kirsten ; Foo, Shen Yun ; Hansbro, Nicole ; Uematsu, Satoshi ; Akira, Shizuo ; Matthaei, Klaus I ; Rosenberg, Helene F ; Foster, Paul S ; Phipps, Simon
Subjects: Adaptive Immunity ; Adoptive Transfer ; Animals ; Dendritic Cells - immunology ; Human respiratory syncytial virus ; Interferons - genetics ; Interferons - immunology ; Membrane Glycoproteins - genetics ; Membrane Glycoproteins - immunology ; Membrane Glycoproteins - metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; Murine pneumonia virus - immunology ; Myeloid Differentiation Factor 88 - genetics ; Myeloid Differentiation Factor 88 - metabolism ; Pneumonia virus of mice ; Pneumovirus ; Pneumovirus Infections - immunology ; Respiratory syncytial virus ; Signal Transduction ; Toll-Like Receptor 7 - genetics ; Toll-Like Receptor 7 - immunology ; Toll-Like Receptor 7 - metabolism
Is Part Of: The Journal of immunology (1950), 2011-05, Vol.186 (10), p.5938-5948
Description: Human respiratory syncytial virus (RSV) is the leading cause of lower respiratory tract infection in infants. In human infants, plasmacytoid dendritic cells (pDC) are recruited to the nasal compartment during infection and initiate host defense through the secretion of type I IFN, IL-12, and IL-6. However, RSV-infected pDC are refractory to TLR7-mediated activation. In this study, we used the rodent-specific pathogen, pneumonia virus of mice (PVM), to determine the contribution of pDC and TLR7 signaling to the development of the innate inflammatory and early adaptive immune response. In wild-type, but not TLR7- or MyD88-deficient mice, PVM inoculation led to a marked infiltration of pDC and increased expression of type I, II, and III IFNs. The delayed induction of IFNs in the absence of TLR7 or MyD88 was associated with a diminished innate inflammatory response and augmented virus recovery from lung tissue. In the absence of TLR7, PVM-specific CD8(+) T cell cytokine production was abrogated. The adoptive transfer of TLR7-sufficient, but not TLR7-deficient pDC to TLR7 gene-deleted mice recapitulated the antiviral responses observed in wild-type mice and promoted virus clearance. In summary, TLR7-mediated signaling by pDC is required for appropriate innate responses to acute pneumovirus infection. It is conceivable that as-yet-unidentified defects in the TLR7 signaling pathway may be associated with elevated levels of RSV-associated morbidity and mortality among otherwise healthy human infants.
Publisher: United States
Language: English
Identifier: ISSN: 0022-1767
EISSN: 1550-6606
DOI: 10.4049/jimmunol.1002635
PMID: 21482736
Source: Geneva Foundation Free Medical Journals at publisher websites
MEDLINE
Alma/SFX Local Collection

Back to results list


INSPIRE LIBRARY - TON DUC THANG UNIVERSITY	(84-028) 37 755 057	Feedback
19 Nguyen Huu Tho St. Dist.7, HCM	thuvien@tdtu.edu.vn	Feedback

Plasmacytoid dendritic cells promote host defense against acute pneumovirus infection via the TLR7-MyD88-dependent signaling pathway

ISSN: 0022-1767 ;EISSN: 1550-6606 ;DOI: 10.4049/jimmunol.1002635 ;PMID: 21482736

Searching Remote Databases, Please Wait