Targeting of antigen to the herpesvirus entry mediator augments primary adaptive immune responses.
Nat Med
; 14(2): 205-12, 2008 Feb.
Article
em En
| MEDLINE
| ID: mdl-18193057
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.
Texto completo:
1
Coleções:
01-internacional
Contexto em Saúde:
2_ODS3
Base de dados:
MEDLINE
Assunto principal:
Membro 14 de Receptores do Fator de Necrose Tumoral
/
Imunidade
/
Antígenos Virais
Limite:
Animals
/
Humans
Idioma:
En
Revista:
Nat Med
Ano de publicação:
2008
Tipo de documento:
Article