Patents by Inventor Carl De Trez

Carl De Trez has filed for patents to protect the following inventions. This listing includes patent applications that are pending as well as patents that have already been granted by the United States Patent and Trademark Office (USPTO).

  • Patent number: 8349320
    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.
    Type: Grant
    Filed: June 10, 2009
    Date of Patent: January 8, 2013
    Assignee: La Jolla Institute for Allergy and Immunology
    Inventors: Carl F. Ware, Carl De Trez, Michael Croft, Timothy C. Cheung, Ian R. Humphreys, Karen G. Potter, Christopher A. Benedict, Mitchell Kronenberg, Marcos W. Steinberg
  • Patent number: 8153123
    Abstract: The present invention provides methods for restoring and increasing dendritic cell populations in a subject by modulation of the lymphotoxin-? receptor (LT?R) via LT?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?R agonist.
    Type: Grant
    Filed: June 11, 2009
    Date of Patent: April 10, 2012
    Assignee: La Jolla Institute for Allergy and Immunology
    Inventors: Carl F. Ware, Carl De Trez
  • Publication number: 20100104559
    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.
    Type: Application
    Filed: June 10, 2009
    Publication date: April 29, 2010
    Inventors: Carl F. Ware, Carl De Trez, Michael Croft, Timothy C. Cheung, Ian R. Humphreys, Karen G. Porter, Christopher A. Benedict, Mitchell Kronenberg, Marcos W. Steinberg
  • Publication number: 20100034815
    Abstract: The present invention provides methods for restoring and increasing dendritic cell populations in a subject by modulation of the lymphotoxin-? receptor (LT?R) via LT?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?R agonist.
    Type: Application
    Filed: June 11, 2009
    Publication date: February 11, 2010
    Applicant: La Jolla Institute For Allergy and Immunology
    Inventors: Carl F. Ware, Carl De Trez
  • Publication number: 20090311280
    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.
    Type: Application
    Filed: December 9, 2005
    Publication date: December 17, 2009
    Applicant: LA JOLLA INSTITUTE FOR ALLERGY AND IMMUNOLOGY
    Inventors: Timothy C. Cheung, Ian R. Humphreys, Karen G. Potter, Christopher A. Benedict, Carl F. Ware, Carl De Trez, Michael Croft, Mitchell Kronenberg