CpG-ODN-induced sustained expression of BTLA mediating selective inhibition of human B cells.

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Version: Final published version
Serval ID
serval:BIB_41EC0257E313
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
CpG-ODN-induced sustained expression of BTLA mediating selective inhibition of human B cells.
Journal
Journal of Molecular Medicine
Author(s)
Thibult M.L., Rivals J.P., Mamessier E., Gertner-Dardenne J., Pastor S., Speiser D.E., Derré L., Olive D.
ISSN
1432-1440 (Electronic)
ISSN-L
0946-2716
Publication state
Published
Issued date
2013
Volume
91
Number
2
Pages
195-205
Language
english
Notes
Publication types: Journal Article Publication Status: ppublish PDF type: Article
Abstract
BTLA (B- and T-lymphocyte attenuator) is a prominent co-receptor that is structurally and functionally related to CTLA-4 and PD-1. In T cells, BTLA inhibits TCR-mediated activation. In B cells, roles and functions of BTLA are still poorly understood and have never been studied in the context of B cells activated by CpG via TLR9. In this study, we evaluated the expression of BTLA depending on activation and differentiation of human B cell subsets in peripheral blood and lymph nodes. Stimulation with CpG upregulated BTLA, but not its ligand: herpes virus entry mediator (HVEM), on B cells in vitro and sustained its expression in vivo in melanoma patients after vaccination. Upon ligation with HVEM, BTLA inhibited CpG-mediated B cell functions (proliferation, cytokine production, and upregulation of co-stimulatory molecules), which was reversed by blocking BTLA/HVEM interactions. Interestingly, chemokine secretion (IL-8 and MIP1β) was not affected by BTLA/HVEM ligation, suggesting that BTLA-mediated inhibition is selective for some but not all B cell functions. We conclude that BTLA is an important immune checkpoint for B cells, as similarly known for T cells.
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Web of science
Create date
01/03/2013 18:56
Last modification date
20/08/2019 14:43
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