La Jolla Institute for Allergy and Immunology

Christopher A Benedict

Carl F Ware

Michael Croft

Marcos Steinberg

Timothy C Cheung

Carl De Trez

Ian R Humphreys

Karen G Potter

Mitchell Kronenberg

Herpesvirus entry mediator (HVEM) is a member of the tumor necrosis factor receptor superfamily (TNFRSF) and acts as a molecular switch that modulates T cell activation by propagating positive signals from the TNF related ligand, LIGHT (p30, TNFSF14), or inhibitory signals through the immunoglobulin superfamily member, B and T lymphocyte attenuator (BTLA). A novel binding site for BTLA is disclosed, located in cysteine-rich domain-1 of HVEM. BTLA binding site on HVEM overlaps with the binding site for the Herpes Simplex virus-1 envelope glycoprotein D (gD), but is distinct from where LIGHT binds, yet gD inhibits the binding of both ligands. A BTLA activating protein present in human cytomegalovirus is identified as UL144. UL144 binds BTLA, but not LIGHT, and inhibits T cell proliferation.

Compositions and methods for modulating responses mediated or associated with BTLA activity

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Encinitas, CA, United States of America

Christopher A Benedict