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Tagawa, T. ; Albanese, M. ; Bouvet, M. ; Moosmann, A. ; Mautner, J. ; Heissmeyer, V. ; Zielinski, C.* ; Lutter, D. ; Hoser, J.D.S. ; Hastreiter, M. ; Hayes, M.* ; Sugden, B.* ; Hammerschmidt, W.

Epstein-Barr viral miRNAs inhibit antiviral CD4+ T cell responses targeting IL-12 and peptide processing.

J. Exp. Med. 213, 2065-2080 (2016)
Verlagsversion Forschungsdaten DOI PMC
Creative Commons Lizenzvertrag
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Epstein-Barr virus (EBV) is a tumor virus that establishes lifelong infection in most of humanity, despite eliciting strong and stable virus-specific immune responses. EBV encodes at least 44 miRNAs, most of them with unknown function. Here, we show that multiple EBV miRNAs modulate immune recognition of recently infected primary B cells, EBV's natural target cells. EBV miRNAs collectively and specifically suppress release of proinflammatory cytokines such as IL-12, repress differentiation of naive CD4(+) T cells to Th1 cells, interfere with peptide processing and presentation on HLA class II, and thus reduce activation of cytotoxic EBV-specific CD4(+) effector T cells and killing of infected B cells. Our findings identify a previously unknown viral strategy of immune evasion. By rapidly expressing multiple miRNAs, which are themselves nonimmunogenic, EBV counteracts recognition by CD4(+) T cells and establishes a program of reduced immunogenicity in recently infected B cells, allowing the virus to express viral proteins required for establishment of life-long infection.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Human B-cells; Virus Infection; Immune Evasion; Lymphoproliferative Disorders; Micrornas Target; Ebv; Recognition; Lymphocytes; Herpesvirus; Expression
ISSN (print) / ISBN 0022-1007
e-ISSN 1540-9538
Zeitschrift Journal of Experimental Medicine
Quellenangaben Band: 213, Heft: 10, Seiten: 2065-2080 Artikelnummer: , Supplement: ,
Verlag Rockefeller University Press
Verlagsort New York
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Research Unit Gene Vector (AGV)
Abteilung für Molekulare Immunregulation (AMIR)
Institute of Diabetes and Obesity (IDO)
Institute of Bioinformatics and Systems Biology (IBIS)