TCF1(+) hepatitis C virus-specific CD8(+) T cells are maintained after cessation of chronic antigen stimulation.

Détails

Ressource 1Télécharger: ncomms15050.pdf (1227.59 [Ko])
Etat: Public
Version: Final published version
Licence: Non spécifiée
ID Serval
serval:BIB_BC4DAD6A8908
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
TCF1(+) hepatitis C virus-specific CD8(+) T cells are maintained after cessation of chronic antigen stimulation.
Périodique
Nature communications
Auteur⸱e⸱s
Wieland D., Kemming J., Schuch A., Emmerich F., Knolle P., Neumann-Haefelin C., Held W., Zehn D., Hofmann M., Thimme R.
ISSN
2041-1723 (Electronic)
ISSN-L
2041-1723
Statut éditorial
Publié
Date de publication
03/05/2017
Peer-reviewed
Oui
Volume
8
Pages
15050
Langue
anglais
Notes
Publication types: Journal Article
Publication Status: epublish
Résumé
Differentiation and fate of virus-specific CD8(+) T cells after cessation of chronic antigen stimulation is unclear. Here we show that a TCF1(+)CD127(+)PD1(+) hepatitis C virus (HCV)-specific CD8(+) T-cell subset exists in chronically infected patients with phenotypic features of T-cell exhaustion and memory, both before and after treatment with direct acting antiviral (DAA) agents. This subset is maintained during, and for a long duration after, HCV elimination. After antigen re-challenge the less differentiated TCF1(+)CD127(+)PD1(+) population expands, which is accompanied by emergence of terminally exhausted TCF1-CD127-PD1(hi) HCV-specific CD8(+) T cells. These results suggest the TCF1(+)CD127(+)PD1(+) HCV-specific CD8(+) T-cell subset has memory-like characteristics, including antigen-independent survival and recall proliferation. We thus provide evidence for the establishment of memory-like virus-specific CD8(+) T cells in a clinically relevant setting of chronic viral infection and we uncover their fate after cessation of chronic antigen stimulation, implicating a potential strategy for antiviral immunotherapy.
Pubmed
Web of science
Open Access
Oui
Création de la notice
09/05/2017 17:57
Dernière modification de la notice
21/11/2022 9:20
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