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Albanese, M. ; Tagawa, T. ; Bouvet, M. ; Maliqi, L. ; Lutter, D. ; Hoser, J.D.S. ; Hastreiter, M. ; Hayes, M.* ; Sugden, B.* ; Martin, L. ; Moosmann, A. ; Hammerschmidt, W.

Epstein-Barr virus microRNAs reduce immune surveillance by virus-specific CD8+ T cells.

Proc. Natl. Acad. Sci. U.S.A. 113, E6467-E6475 (2016)
Verlagsversion Forschungsdaten DOI PMC
Open Access Gold
Infection with Epstein-Barr virus (EBV) affects most humans worldwide and persists life-long in the presence of robust virus-specific T-cell responses. In both immunocompromised and some immunocompetent people, EBV causes several cancers and lymphoproliferative diseases. EBV transforms B cells in vitro and encodes at least 44 microRNAs (miRNAs), most of which are expressed in EBV-transformed B cells, but their functions are largely unknown. Recently, we showed that EBV miRNAs inhibit CD4(+) T-cell responses to infected B cells by targeting IL-12, MHC class II, and lysosomal proteases. Here we investigated whether EBV miRNAs also counteract surveillance by CD8(+) T cells. We have found that EBV miRNAs strongly inhibit recognition and killing of infected B cells by EBV-specific CD8(+) T cells through multiple mechanisms. EBV miRNAs directly target the peptide transporter subunit TAP2 and reduce levels of the TAP1 subunit, MHC class I molecules, and EBNA1, a protein expressed in most forms of EBV latency and a target of EBV-specific CD8(+) T cells. Moreover, miRNA-mediated down-regulation of the cytokine IL-12 decreases the recognition of infected cells by EBV-specific CD8(+) T cells. Thus, EBV miRNAs use multiple, distinct pathways, allowing the virus to evade surveillance not only by CD4(+) but also by antiviral CD8(+) T cells.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Cd8 T Cells ; Adaptive Immunity ; Herpesvirus ; Immune Evasion ; Microrna; Lymphoproliferative Disease; B-cells; Antigen Presentation; Encoded Micrornas; Cycle Antigens; Host Shutoff; Lytic Phase; Ebv; Lymphocytes; Responses
Sprache
Veröffentlichungsjahr 2016
HGF-Berichtsjahr 2016
ISSN (print) / ISBN 0027-8424
e-ISSN 1091-6490
Zeitschrift Proceedings of the National Academy of Sciences of the United States of America
Quellenangaben Band: 113, Heft: 42, Seiten: E6467-E6475 Artikelnummer: , Supplement: ,
Verlag National Academy of Sciences
Verlagsort Washington
Begutachtungsstatus Peer reviewed
Institut(e) Research Unit Gene Vector (AGV)
Institute of Diabetes and Obesity (IDO)
Institute of Bioinformatics and Systems Biology (IBIS)
POF Topic(s) 30203 - Molecular Targets and Therapies
30201 - Metabolic Health
30505 - New Technologies for Biomedical Discoveries
Forschungsfeld(er) Immune Response and Infection
Helmholtz Diabetes Center
Enabling and Novel Technologies
PSP-Element(e) G-501500-001
G-502200-001
G-503700-001
DOI 10.1073/pnas.1605884113
WOS ID WOS:000385610400020
Scopus ID 84991666745
PubMed ID 27698133
Erfassungsdatum 2016-10-17
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