Systemic activation of dendritic cells by toll-like receptor ligands or malaria infection impairs cross-presentation and antiviral immunity

Wilson, Nicholas S., Behrens, Georg M., Lundie, Rachel J., Smith, Christopher M., Waithman, Jason, Young, Louise, Forehan, Simon P., Mount, Adele, Steptoe, Raymond J., Shortman, Ken D., de Koning-Ward, Tania F., Belz, Gabrielle T., Carbone, Francis R., Crabb, Brendan S., Heath, William R. and Villadangos, Jose A. 2006, Systemic activation of dendritic cells by toll-like receptor ligands or malaria infection impairs cross-presentation and antiviral immunity, Nature immunology, vol. 7, no. 2, pp. 165-172.


Title Systemic activation of dendritic cells by toll-like receptor ligands or malaria infection impairs cross-presentation and antiviral immunity
Author(s) Wilson, Nicholas S.
Behrens, Georg M.
Lundie, Rachel J.
Smith, Christopher M.
Waithman, Jason
Young, Louise
Forehan, Simon P.
Mount, Adele
Steptoe, Raymond J.
Shortman, Ken D.
de Koning-Ward, Tania F.
Belz, Gabrielle T.
Carbone, Francis R.
Crabb, Brendan S.
Heath, William R.
Villadangos, Jose A.
Journal name Nature immunology
Volume number 7
Issue number 2
Start page 165
End page 172
Publisher Nature Publishing Group
Place of publication New York, N. Y.
Publication date 2006-01-15
ISSN 1529-2908
1529-2916
Summary The mechanisms responsible for the immunosuppression associated with sepsis or some chronic blood infections remain poorly understood. Here we show that infection with a malaria parasite (Plasmodium berghei) or simple systemic exposure to bacterial or viral Toll-like receptor ligands inhibited cross-priming. Reduced cross-priming was a consequence of downregulation of cross-presentation by activated dendritic cells due to systemic activation that did not otherwise globally inhibit T cell proliferation. Although activated dendritic cells retained their capacity to present viral antigens via the endogenous major histocompatibility complex class I processing pathway, antiviral responses were greatly impaired in mice exposed to Toll-like receptor ligands. This is consistent with a key function for cross-presentation in antiviral immunity and helps explain the immunosuppressive effects of systemic infection. Moreover, inhibition of cross-presentation was overcome by injection of dendritic cells bearing antigen, which provides a new strategy for generating immunity during immunosuppressive blood infections.
Language eng
Field of Research 110804 Medical Virology
Socio Economic Objective 970111 Expanding Knowledge in the Medical and Health Sciences
HERDC Research category C1.1 Refereed article in a scholarly journal
Copyright notice ©2006, Nature Publishing Group
Persistent URL http://hdl.handle.net/10536/DRO/DU:30028231

Document type: Journal Article
Collection: School of Medicine
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