La Jolla Institute for Allergy and Immunology

Carl De Trez

Carl F Ware

Michael Croft

Marcos Steinberg

Timothy C Cheung

Ian R Humphreys

Karen G Potter

Christopher A Benedict

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

The present invention provides methods for restoring and increasing dendritic cell populations in a subject by modulation of the lymphotoxin-&#x3b2; receptor (LT&#x3b2;R) via LT&#x3b2;R agonists. The invention also provides methods for screening for agents capable of restoring or increasing dendritic cell populations. The invention further provides a method for the treatment of immunodeficiency by administration of an LT&#x3b2;R agonist.

Method for restoring dendritic cell populations

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Brussels, Belgium

Carl De Trez