Skip Navigation


International Immunology Advance Access originally published online on November 13, 2007
International Immunology 2008 20(1):45-56; doi:10.1093/intimm/dxm119
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
20/1/45    most recent
dxm119v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (8)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Zucchini, N.
Right arrow Articles by Dalod, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zucchini, N.
Right arrow Articles by Dalod, M.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?


© The Japanese Society for Immunology. 2007. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Individual plasmacytoid dendritic cells are major contributors to the production of multiple innate cytokines in an organ-specific manner during viral infection

Nicolas Zucchini1,2,3, Gilles Bessou1,2,3, Scott H. Robbins1,2,3, Lionel Chasson1,2,3, Anna Raper4, Paul R. Crocker4 and Marc Dalod1,2,3

1 Centre d'Immunologie de Marseille-Luminy, Université de la Méditerranée, Case 906, 13288 Marseille cedex 9, France
2 Institut National de la Santé et de la Recherche Médicale, U631, 13288 Marseille, France
3 Centre National de la Recherche Scientifique, UMR6102, 13288 Marseille, France
4 Division of Cell Biology and Immunology, Wellcome Trust Biocentre WTB2, University of Dundee, Dow Street, Dundee DD1 5EH, UK

Correspondence to: M. Dalod; E-mail: dalod{at}ciml.univ-mrs.fr

Plasmacytoid dendritic cells (pDCs) are an important source of IFN-{alpha}/β in response to a variety of viruses in vivo, including murine cytomegalovirus (MCMV). However, the respective contributions of various infected organs, and within these of pDCs, conventional dendritic cells and other cells, to the systemic production of IFN-{alpha}/β or other innate cytokines during viral infections in vivo is largely unknown. Whether a specialization of pDC subsets in the production of different patterns of innate cytokines exists in vivo in response to a viral infection has not been investigated. Here, by analyzing for the first time directly ex vivo, at the single-cell level, the simultaneous production of up to three cytokines in pDCs isolated from MCMV-infected mice, we show that (i) pDCs are the quasi-exclusive source of IFN-{alpha}/β, IL-12 and tumor necrosis factor (TNF)-{alpha}, early during MCMV infection, in two immunocompetent mouse lines and with two viral strains, (ii) pDC activation for IFN-{alpha}/β production is organ specific and (iii) a significant proportion of pDCs simultaneously produce IFN-{alpha}/β, TNF-{alpha} and IL-12, although TNF-{alpha} and IFN-{alpha}/β appear more often co-expressed with one another than each of them with IL-12. Altogether, these results show a broad and non-redundant role of pDCs in early innate detection of, and defense against, viral infection. The data also show differences in the responsiveness of pDCs from different tissues and suggest distinct molecular requirements for pDC production of various cytokines. These observations must be taken into account when designing new antiviral vaccination strategies aimed at harnessing pDC responses.

Keywords: dendritic cells, IFN-{alpha}/β, IL-12, murine cytomegalovirus, tumor necrosis factor-{alpha}

Transmitting editor: G. Trinchieri

Received 5 April 2007, accepted 15 October 2007.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 J. Immunol.Home page
A. Castellaneta, T. L. Sumpter, L. Chen, D. Tokita, and A. W. Thomson
NOD2 Ligation Subverts IFN-{alpha} Production by Liver Plasmacytoid Dendritic Cells and Inhibits Their T Cell Allostimulatory Activity via B7-H1 Up-Regulation
J. Immunol., December 1, 2009; 183(11): 6922 - 6932.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
M. J. Crane, K. L. Hokeness-Antonelli, and T. P. Salazar-Mather
Regulation of Inflammatory Monocyte/Macrophage Recruitment from the Bone Marrow during Murine Cytomegalovirus Infection: Role for Type I Interferons in Localized Induction of CCR2 Ligands
J. Immunol., August 15, 2009; 183(4): 2810 - 2817.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
S. Scheu, P. Dresing, and R. M. Locksley
Visualization of IFN{beta} production by plasmacytoid versus conventional dendritic cells under specific stimulation conditions in vivo
PNAS, December 23, 2008; 105(51): 20416 - 20421.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
N. Fodil-Cornu, S.-H. Lee, S. Belanger, A. P. Makrigiannis, C. A. Biron, R. M. Buller, and S. M. Vidal
Ly49h-Deficient C57BL/6 Mice: A New Mouse Cytomegalovirus-Susceptible Model Remains Resistant to Unrelated Pathogens Controlled by the NK Gene Complex
J. Immunol., November 1, 2008; 181(9): 6394 - 6405.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
N. Sachdeva, V. Asthana, T. H. Brewer, D. Garcia, and D. Asthana
Impaired Restoration of Plasmacytoid Dendritic Cells in HIV-1-Infected Patients with Poor CD4 T Cell Reconstitution Is Associated with Decrease in Capacity to Produce IFN-{alpha} but Not Proinflammatory Cytokines
J. Immunol., August 15, 2008; 181(4): 2887 - 2897.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
N. Zucchini, G. Bessou, S. Traub, S. H. Robbins, S. Uematsu, S. Akira, L. Alexopoulou, and M. Dalod
Cutting Edge: Overlapping Functions of TLR7 and TLR9 for Innate Defense against a Herpesvirus Infection
J. Immunol., May 1, 2008; 180(9): 5799 - 5803.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.