Toll-like receptor 3 promotes cross-priming to virus-infected cells

Oliver Schulz, Sandra S. Diebold, Margaret Chen, Tanja I. Näslund, Martijn A. Nolte, Lena Alexopoulou, Yasu-Taka Azuma, Richard A. Flavell, Peter Liljeström and Caetano Reis e Sousa ()
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Oliver Schulz: Cancer Research UK London Research Institute, Lincoln's Inn Fields Laboratories
Sandra S. Diebold: Cancer Research UK London Research Institute, Lincoln's Inn Fields Laboratories
Margaret Chen: Karolinska Institutet
Tanja I. Näslund: Karolinska Institutet
Martijn A. Nolte: Cancer Research UK London Research Institute, Lincoln's Inn Fields Laboratories
Lena Alexopoulou: Yale University School of Medicine and Howard Hughes Medical Institute
Yasu-Taka Azuma: Yale University School of Medicine and Howard Hughes Medical Institute
Richard A. Flavell: Yale University School of Medicine and Howard Hughes Medical Institute
Peter Liljeström: Karolinska Institutet
Caetano Reis e Sousa: Cancer Research UK London Research Institute, Lincoln's Inn Fields Laboratories

Nature, 2005, vol. 433, issue 7028, 887-892

Abstract: Abstract Cross-presentation of cell-associated antigens plays an important role in regulating CD8+ T cell responses to proteins that are not expressed by antigen-presenting cells (APCs)1. Dendritic cells are the principal cross-presenting APCs in vivo and much progress has been made in elucidating the pathways that allow dendritic cells to capture and process cellular material1. However, little is known about the signals that determine whether such presentation ultimately results in a cytotoxic T cell (CTL) response (cross-priming) or in CD8+ T cell inactivation (cross-tolerance). Here we describe a mechanism that promotes cross-priming during viral infections. We show that murine CD8α+ dendritic cells are activated by double-stranded (ds)RNA present in virally infected cells but absent from uninfected cells. Dendritic cell activation requires phagocytosis of infected material, followed by signalling through the dsRNA receptor, toll-like receptor 3 (TLR3). Immunization with virus-infected cells or cells containing synthetic dsRNA leads to a striking increase in CTL cross-priming against cell-associated antigens, which is largely dependent on TLR3 expression by antigen-presenting cells. Thus, TLR3 may have evolved to permit cross-priming of CTLs against viruses that do not directly infect dendritic cells.

Date: 2005
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DOI: 10.1038/nature03326

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