Immune escape pathways from the HBV core
CD8 T cell response
TCR-engineered T cells
chronic infection
hepatitis B virus
immune escape
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2022
2022
Historique:
received:
15
09
2022
accepted:
19
10
2022
entrez:
28
11
2022
pubmed:
29
11
2022
medline:
30
11
2022
Statut:
epublish
Résumé
There is growing interest in T cell-based immune therapies for a functional cure of chronic HBV infection including check-point inhibition, T cell-targeted vaccines or TCR-grafted effector cells. All these approaches depend on recognition of HLA class I-presented viral peptides. The HBV core region 18-27 is an immunodominant target of CD8+ T cells and represents the prime target for T cell-based therapies. Here, a high-resolution analysis of the core HLA class I typing and viral sequence analyses were performed for 464 patients with chronic HBV infection. HBV-specific CD8+ T-cell responses against the prototype and epitope variants were characterized by flow cytometry. Consistent with promiscuous presentation of the core The core
Sections du résumé
Background and aims
There is growing interest in T cell-based immune therapies for a functional cure of chronic HBV infection including check-point inhibition, T cell-targeted vaccines or TCR-grafted effector cells. All these approaches depend on recognition of HLA class I-presented viral peptides. The HBV core region 18-27 is an immunodominant target of CD8+ T cells and represents the prime target for T cell-based therapies. Here, a high-resolution analysis of the core
Methods
HLA class I typing and viral sequence analyses were performed for 464 patients with chronic HBV infection. HBV-specific CD8+ T-cell responses against the prototype and epitope variants were characterized by flow cytometry.
Results
Consistent with promiscuous presentation of the core
Conclusion
The core
Identifiants
pubmed: 36439181
doi: 10.3389/fimmu.2022.1045498
pmc: PMC9686862
doi:
Substances chimiques
HLA-B Antigens
0
Epitopes
0
Receptors, Antigen, T-Cell
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1045498Subventions
Organisme : Medical Research Council
ID : G0901374
Pays : United Kingdom
Informations de copyright
Copyright © 2022 Walker, Schwarz, Brinkmann-Paulukat, Wisskirchen, Menne, Alizei, Kefalakes, Theissen, Hoffmann, Schulze zur Wiesch, Maini, Cornberg, Kraft, Keitel, Bock, Horn, Thimme, Wedemeyer, Heinemann, Luedde, Neumann-Haefelin, Protzer and Timm.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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