Systemic activation of dendritic cells by Toll-like receptor ligands or malaria infection impairs cross-presentation and antiviral immunity View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2006-02

AUTHORS

Nicholas S Wilson, Georg M N Behrens, Rachel J Lundie, Christopher M Smith, Jason Waithman, Louise Young, Simon P Forehan, Adele Mount, Raymond J Steptoe, Ken D Shortman, Tania F de Koning-Ward, Gabrielle T Belz, Francis R Carbone, Brendan S Crabb, William R Heath, Jose A Villadangos

ABSTRACT

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. More... »

PAGES

165-172

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ni1300

DOI

http://dx.doi.org/10.1038/ni1300

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1050070379

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/16415871


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