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Article Dans Une Revue Nature Année : 2005

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

Oliver Schulz
  • Fonction : Auteur
Sandra S Diebold
  • Fonction : Auteur
Margaret Chen
  • Fonction : Auteur
Tanja I Näslund
  • Fonction : Auteur
Martijn A Nolte
  • Fonction : Auteur
Yasu-Taka Azuma
  • Fonction : Auteur
Richard A Flavell
  • Fonction : Auteur
Peter Liljeström
  • Fonction : Auteur
Caetano Reis E Sousa
  • Fonction : Auteur

Résumé

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). 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 material. 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 CD8alpha+ 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.

Domaines

Immunologie

Dates et versions

hal-00165709 , version 1 (27-07-2007)

Identifiants

Citer

Oliver Schulz, Sandra S Diebold, Margaret Chen, Tanja I Näslund, Martijn A Nolte, et al.. Toll-like receptor 3 promotes cross-priming to virus-infected cells.. Nature, 2005, 433 (7028), pp.887-92. ⟨10.1038/nature03326⟩. ⟨hal-00165709⟩

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