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Nat Med. 2008 Feb;14(2):205-12. doi: 10.1038/nm1704. Epub 2008 Jan 13.

Targeting of antigen to the herpesvirus entry mediator augments primary adaptive immune responses.

Author information

1
The Wistar Institute, 3601 Spruce Street, Philadelphia, Pennsylvania 19104, USA.

Abstract

Interactions between the herpesvirus entry mediator (HVEM) and the B- and T-lymphocyte attenuator (BTLA) inhibit B and T cell activation. HVEM-BTLA interactions are blocked by herpes simplex virus (HSV) glycoprotein D (gD) through binding of its N-terminal domain to the BTLA binding site of HVEM. In this study, we inserted viral antigens into the C-terminal domain of gD and expressed these antigens with plasmid or E1-deleted (replication-defective) adenovirus vectors. Viral antigens fused to gD induced T and B cell responses to the antigen that were far more potent than those elicited by the same antigen expressed without gD. The immunopotentiating effect required binding of the gD chimeric protein to HVEM. Overall, the studies demonstrate that targeting of antigen to the BTLA binding site of HVEM augments the immunogenicity of vaccines.

PMID:
18193057
PMCID:
PMC3992986
DOI:
10.1038/nm1704
[Indexed for MEDLINE]
Free PMC Article

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