Compositions and methods for modulating responses mediated or associated with BTLA activity
US8349320B2 · kind B2 · utility
Assignee
Inventors
Key dates
| Filing date | Jun 10, 2009 |
| Grant date | Jan 8, 2013 |
| Priority date | — |
| Expiry date | Mar 2, 2030 |
Classification
- Technology area (CPC C)Chemistry; Metallurgy
- CPC primaryC07K2317/73
- WIPO fieldPharmaceuticals
- WIPO sectorChemistry
Abstract
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.
Source: USPTO / EPO open patent data. Objective bibliographic and citation counts.