HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Coppieters, K. Articles by von Herrath, M. G. Search for Related Content PubMed PubMed Citation Articles by Coppieters, K. Articles by von Herrath, M. G.

No Significant CTL Cross-Priming by Dendritic Cell-Derived Exosomes during Murine Lymphocytic Choriomeningitis Virus Infection¹

Ken Coppieters^*, Ana María Barral^*, Amy Juedes^*, Tom Wolfe^*, Evelyn Rodrigo^*, Clotilde Théry, Sebastian Amigorena and Matthias G. von Herrath^2,*

^* Immune Regulation Laboratory DI-3, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037; and Institut Curie, Centre de Recherche, Paris, France and Institut National de la Santé et de la Recherche Médicale U653, Immunité et Cancer, Paris, France

Exosomes are small membrane vesicles of endocytic origin that are secreted by most cells in culture, but are also present in serum. They contain a wide array of protein ligands on their surface, which has led to the hypothesis that they might mediate intercellular communication. Indeed, data support that exosomes can transfer Ags to dendritic cells (DC), and, interestingly, that these DC can subsequently induce T cell priming or tolerance. We have investigated whether this concept can be expanded to antiviral immunity. We isolated exosomes from supernatant of cultured bone marrow-derived DC (BMDC) that were infected with lymphocytic choriomeningitis virus (LCMV) or loaded with an immunodominant LCMV peptide, and characterized them by flow cytometry upon binding to beads. We then incubated the exosome preparations with BMDC and looked at their potential to activate LCMV gp33-specific naive and memory CD8 T cells. We found that exosomes do not significantly contribute to CD8 T cell cross-priming in vitro. Additionally, exosomes derived from in vitro-infected BMDC did not exhibit significant in vivo priming activity, as evidenced by the lack of protection following exosome vaccination. Thus, DC-derived exosomes do not appear to contribute significantly to CTL priming during acute LCMV infection.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ K.C. is supported by the D. Collen Research Foundation, the Belgian American Educational Foundation, and the Commission for Educational Exchange between the United States of America, Belgium, and Luxembourg (The Fulbright Program).

² Address correspondence and reprint requests to Dr. Matthias G. Von Herat, Immune Regulation Laboratory DI-3, La Jolla Institute for Allergy and Immunology, 9420 Athena Circle, La Jolla, CA 92037. E-mail address: matthias{at}liai.org

³ Abbreviations used in this paper: DC, dendritic cells; BMDC, bone marrow-derived dendritic cells; i.c., intracranially; imDC, immature DC; mDC, LPS-matured DC; LCMV, lymphocytic choriomeningitis virus; PD-1, programmed death-1; PD-L1, PD ligand 1; PD-L2, PD ligand 2.