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Hantaviral mechanisms driving HLA class I antigen presentation require both RIG-I and TRIF

Hantaviruses are emerging human pathogens. They induce an unusually strong antiviral response of human HLA class I (HLA-I) restricted CD8+ T cells that may contribute to tissue damage and hantavirus-associated disease. In this study, we analyzed possible hantaviral mechanisms that enhance the HLA-I...

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Hauptverfasser: Lalwani, Pritesh Jaychand (VerfasserIn) , Raftery, Martin J. (VerfasserIn) , Kobak, Lidija (VerfasserIn) , Rang, Andreas (VerfasserIn) , Giese, Thomas (VerfasserIn) , Matthaei, Markus (VerfasserIn) , van den Elsen, Peter J. (VerfasserIn) , Wolff, Thorsten (VerfasserIn) , Krüger, Detlev H. (VerfasserIn) , Schönrich, Günther (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: 4/7/2013
In: European journal of immunology
Year: 2013, Jahrgang: 43, Heft: 10, Pages: 2566-2576
ISSN:1521-4141
DOI:10.1002/eji.201243066
Online-Zugang:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1002/eji.201243066
Verlag, lizenzpflichtig, Volltext: https://onlinelibrary.wiley.com/doi/abs/10.1002/eji.201243066
Volltext
Verfasserangaben:Pritesh Lalwani, Martin J. Raftery, Lidija Kobak, Andreas Rang, Thomas Giese, Markus Matthaei, Peter J. van den Elsen, Thorsten Wolff, Detlev H. Krüger and Günther Schönrich
Beschreibung
Zusammenfassung:Hantaviruses are emerging human pathogens. They induce an unusually strong antiviral response of human HLA class I (HLA-I) restricted CD8+ T cells that may contribute to tissue damage and hantavirus-associated disease. In this study, we analyzed possible hantaviral mechanisms that enhance the HLA-I antigen presentation machinery. Upon hantavirus infection of various human and primate cell lines, we observed transactivation of promoters controlling classical HLA molecules. Hantavirus-induced HLA-I upregulation required proteasomal activity and was associated with increased TAP expression. Intriguingly, human DCs acquired the capacity to cross-present antigen upon hantavirus infection. Furthermore, knockdown of TIR domain containing adaptor inducing IFN-β or retinoic acid inducible gene I abolished hantavirus-driven HLA-I induction. In contrast, MyD88-dependent viral sensors were not involved in HLA-I induction. Our results show that hantaviruses strongly boost the HLA-I antigen presentation machinery by mechanisms that are dependent on both retinoic acid inducible gene I and TIR domain containing adaptor inducing IFN-β.
Beschreibung:Gesehen am 22.09.2021
Beschreibung:Online Resource
ISSN:1521-4141
DOI:10.1002/eji.201243066

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