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: | , , , , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
4/7/2013
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| 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 
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| 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 |
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| 245 | 1 | 0 | |a Hantaviral mechanisms driving HLA class I antigen presentation require both RIG-I and TRIF |c 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 |
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| 520 | |a 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. | ||
| 650 | 4 | |a Antigen presentation/processing | |
| 650 | 4 | |a Cross-presentation/priming | |
| 650 | 4 | |a Immunopathology | |
| 650 | 4 | |a Infectious diseases | |
| 650 | 4 | |a Innate immunity | |
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