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

Nature Medicine
Marcio O LasaroHildegund C J Ertl

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.

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Citations

Jun 11, 2009·Molecular Therapy : the Journal of the American Society of Gene Therapy·Marcio O Lasaro, Hildegund C J Ertl
Dec 16, 2010·Molecular Therapy : the Journal of the American Society of Gene Therapy·Hua LiHildegund C J Ertl
May 19, 2011·Molecular Therapy : the Journal of the American Society of Gene Therapy·Marcio O LasaroHildegund Cj Ertl
Oct 30, 2010·Nature Protocols·Dongming ZhouHildegund C J Ertl
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May 15, 2010·Current Opinion in Immunology·Marcio O Lasaro, Hildegund C J Ertl
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