Patents by Inventor Carl F. Ware
Carl F. Ware 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).
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Publication number: 20130230536Abstract: Provided herein are antibodies that immunospecifically bind to an hLIGHT polypeptide; isolated nucleic acids encoding the antibodies; vectors and host cells comprising nucleic acids encoding the antibodies; methods of making the antibodies; and a method of treating a hLIGHT-mediated disease in a subject comprising administering to the subject the antibodies. In preferred embodiments, the anti-hLIGHT antibodies provided herein will ameliorate, neutralize or otherwise inhibit hLIGHT biological activity in vivo (e.g., the hLIGHT-mediated production or secretion of CCL20, IL-8 or RANTES from a cell expressing a hLIGHT receptor). Also provided herein is a method for the detection of hLIGHT in a sample as well as a method for ameliorating, neutralizing or otherwise inhibiting hLIGHT activity, e.g., in a human subject suffering from a disorder in which hLIGHT activity is detrimental.Type: ApplicationFiled: May 8, 2013Publication date: September 5, 2013Applicants: La Jolla Institute for Allergy and Immunology, Kyowa Hakko Kirin Co., LimitedInventors: Steven W. Granger, Shinichiro Kato, Carl F. Ware
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Patent number: 8461307Abstract: Provided herein are antibodies that immunospecifically bind to an hLIGHT polypeptide; isolated nucleic acids encoding the antibodies; vectors and host cells comprising nucleic acids encoding the antibodies; methods of making the antibodies; and a method of treating a hLIGHT-mediated disease in a subject comprising administering to the subject the antibodies. In preferred embodiments, the anti-hLIGHT antibodies provided herein will ameliorate, neutralize or otherwise inhibit hLIGHT biological activity in vivo (e.g., the hLIGHT-mediated production or secretion of CCL20, IL-8 or RANTES from a cell expressing a hLIGHT receptor). Also provided herein is a method for the detection of hLIGHT in a sample as well as a method for ameliorating, neutralizing or otherwise inhibiting hLIGHT activity, e.g., in a human subject suffering from a disorder in which hLIGHT activity is detrimental.Type: GrantFiled: September 22, 2011Date of Patent: June 11, 2013Assignees: Kyowa Hakko Kirin Co., Limited, La Jolla Institute for Allergy and ImmunologyInventors: Steven W. Granger, Shinichiro Kato, Carl F. Ware
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Patent number: 8349320Abstract: 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: GrantFiled: June 10, 2009Date of Patent: January 8, 2013Assignee: La Jolla Institute for Allergy and ImmunologyInventors: 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
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Publication number: 20120251505Abstract: The invention provides human lymphoid tissue inducer (LTi) cells, methods of producing human lymphoid tissue inducer (LTi) cells, and methods of using human lymphoid tissue inducer (LTi) cells. Such methods include treatment of a subject that would benefit from human lymphoid tissue inducer (LTi) cells, for example, an immunocompromised or immunosuppressed subject.Type: ApplicationFiled: September 3, 2010Publication date: October 4, 2012Applicant: La Jolla Institute for Allergy and ImmunologyInventors: Carl F. Ware, Vasileios Bekiaris
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Publication number: 20120141465Abstract: The invention relates to compositions and methods that employ OX40 (CD134), a TNFR superfamily protein, agonists. The invention includes among other things administering an OX40 agonist alone or in combination with a viral antigen, or live or attenuated virus, to treat a viral infection, or for vaccination or immunization.Type: ApplicationFiled: October 4, 2007Publication date: June 7, 2012Applicant: La Jolla Institute for Allergy and ImmunologyInventors: MICHAEL CROFT, Shahram Salek-Ardakani, Magdalini Moutaftsi, Alessandro Sette, Carl F. Ware
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Patent number: 8153123Abstract: 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: GrantFiled: June 11, 2009Date of Patent: April 10, 2012Assignee: La Jolla Institute for Allergy and ImmunologyInventors: Carl F. Ware, Carl De Trez
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Publication number: 20120076798Abstract: Provided herein are antibodies that immunospecifically bind to an hLIGHT polypeptide; isolated nucleic acids encoding the antibodies; vectors and host cells comprising nucleic acids encoding the antibodies; methods of making the antibodies; and a method of treating a hLIGHT-mediated disease in a subject comprising administering to the subject the antibodies. In preferred embodiments, the anti-hLIGHT antibodies provided herein will ameliorate, neutralize or otherwise inhibit hLIGHT biological activity in vivo (e.g., the hLIGHT-mediated production or secretion of CCL20, IL-8 or RANTES from a cell expressing a hLIGHT receptor). Also provided herein is a method for the detection of hLIGHT in a sample as well as a method for ameliorating, neutralizing or otherwise inhibiting hLIGHT activity, e.g., in a human subject suffering from a disorder in which hLIGHT activity is detrimental.Type: ApplicationFiled: September 22, 2011Publication date: March 29, 2012Applicants: LA JOLLA INSTITUTE FOR ALLERGY AND IMMUNOLOGY, KYOWA HAKKO KIRIN CO., LIMITEDInventors: Steven W. Granger, Shinichiro Kato, Carl F. Ware
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Patent number: 8058402Abstract: Provided herein are antibodies, such as fully human antibodies that immunospecifically bind to an hLIGHT polypeptide. Also provided are isolated nucleic acids encoding antibodies, such as fully human antibodies, that immunospecifically bind to a hLIGHT polypeptide. Further provided are vectors and host cells comprising nucleic acids encoding antibodies, such as fully human antibodies, that immunospecifically bind to a hLIGHT polypeptide. Also provided are methods of making antibodies, such as fully human antibodies, that immunospecifically bind to a hLIGHT polypeptide. Also provided herein is a method of treating a hLIGHT-mediated disease in a subject comprising administering to the subject an antibody, such as a fully human antibody, that immunospecifically binds to a hLIGHT polypeptide. In preferred embodiments, that anti-hLIGHT antibodies provided herein will ameliorate, neutralize or otherwise inhibit hLIGHT biological activity in vivo (e.g.Type: GrantFiled: August 24, 2007Date of Patent: November 15, 2011Assignees: Kyowa Hakko Kirin, La Jolla Institute for Allergy and ImmunologyInventors: Steven W. Granger, Shinichiro Kato, Carl F. Ware
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Publication number: 20110123551Abstract: The invention provides HVEM cis complexes which include, for example, HVEM/BTLA, HVEM/CD160 and HVEM/gD cis complexes. The invention provides ligands and agents that bind to HVEM cis complexes, such as antibodies. The invention further provides methods of use of the HVEM cis complexes, and the ligands and agents (e.g., antibodies) that bind to the HVEM cis complexes.Type: ApplicationFiled: July 8, 2009Publication date: May 26, 2011Inventors: Carl F. Ware, Timothy C. Cheung, Marcos W. Steinberg
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Publication number: 20100136061Abstract: The tumor-necrosis factor superfamily member LIGHT (p30; TNFSF-14) is a cytokine for inducing immune responses against tumors. A novel biochemical approach is used to decorate the surface of tumor cells with LIGHT. LIGHT decorated cells can be used to vaccinate and induce effective, sustained immunity against cells expressing neo or pathogen associated antigens. Variants of LIGHT are described that enhance binding to cellular receptors (e.g., LT beta receptor) and decrease regulation by inhibitors (e.g., Decoy Receptor 3) increasing ability to stimulate immunity.Type: ApplicationFiled: October 25, 2007Publication date: June 3, 2010Applicant: LA JOLLA INSTITUTE FOR ALLERGY AND IMMUNOLOGYInventors: Carl F. Ware, Timothy C. Cheung, Theresia A. Banks
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Publication number: 20100129389Abstract: The invention provides HVEM cis complexes which include, for example, HVEM/BTLA, HVEM/CD160 and HVEM/gD cis complexes. The invention provides ligands and agents that bind to HVEM cis complexes, such as antibodies. The invention further provides methods of use of the HVEM cis complexes, and the ligands and agents (e.g., LIGHT polypeptide sequence) that bind to the HVEM cis complexes.Type: ApplicationFiled: August 3, 2009Publication date: May 27, 2010Applicant: LA JOLLA INSTITUTE FOR ALLERGY AND IMMUNOLOGYInventors: CARL F. WARE, Timothy C. Cheung, Marcos Steinberg
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Publication number: 20100104559Abstract: 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: ApplicationFiled: June 10, 2009Publication date: April 29, 2010Inventors: 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
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Publication number: 20100034815Abstract: 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: ApplicationFiled: June 11, 2009Publication date: February 11, 2010Applicant: La Jolla Institute For Allergy and ImmunologyInventors: Carl F. Ware, Carl De Trez
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Publication number: 20100021466Abstract: Provided herein are antibodies, such as fully human antibodies that immunospecifically bind to an hLIGHT polypeptide. Also provided are isolated nucleic acids encoding antibodies, such as fully human antibodies, that immunospecifically bind to a hLIGHT polypeptide. Further provided are vectors and host cells comprising nucleic acids encoding antibodies, such as fully human antibodies, that immunospecifically bind to a hLIGHT polypeptide. Also provided are methods of making antibodies, such as fully human antibodies, that immunospecifically bind to a hLIGHT polypeptide. Also provided herein is a method of treating a hLIGHT-mediated disease in a subject comprising administering to the subject an antibody, such as a fully human antibody, that immunospecifically binds to a hLIGHT polypeptide. In preferred embodiments, that anti-hLIGHT antibodies provided herein will ameliorate, neutralize or otherwise inhibit hLIGHT biological activity in vivo (e.g.Type: ApplicationFiled: August 24, 2007Publication date: January 28, 2010Inventors: Steven W. Granger, Shinichiro Kato, Carl F. Ware
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Publication number: 20090311280Abstract: 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: ApplicationFiled: December 9, 2005Publication date: December 17, 2009Applicant: LA JOLLA INSTITUTE FOR ALLERGY AND IMMUNOLOGYInventors: Timothy C. Cheung, Ian R. Humphreys, Karen G. Potter, Christopher A. Benedict, Carl F. Ware, Carl De Trez, Michael Croft, Mitchell Kronenberg
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Patent number: 7575745Abstract: A novel polypeptide ligand, p30, or LIGHT, for herpes virus entry mediator, HVEM, is provided. LIGHT is useful for modulating immune responses and in inhibiting infection and/or subsequent proliferation by herpesvirus. HVEM fusion proteins are also provided. Methods for treating subjects with lymphoid cell disorders, tumors, autoimmune diseases, inflammatory disorders or those having or suspected of having a herpesvirus infection, utilizing p30 and the fusion proteins of the invention, are also provided.Type: GrantFiled: August 29, 2006Date of Patent: August 18, 2009Assignee: La Jolla Institute for Allergy and ImmunologyInventor: Carl F. Ware
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Patent number: 7030080Abstract: This invention relates to lymphotoxin-?, a lymphocyte membrane type protein. This protein is found on the surface of a number of cells, including phorbol ester (PMA) stimulated T cell hybridoma II-23.D7 cells. This invention also relates to complexes formed between lymphotoxin-? and other peptides such as lymphotoxin-? and to complexes comprising multiple subunits of lymphotoxin-?. These proteins and complexes are useful in holding LT-? formed within the cell on the cell surface where the LT-?/LT-? complex may act as an inflammation regulating agent, a tumor growth inhibiting agent, a T cell inhibiting agent, a T cell activating agent, an autoimmune disease regulating agent, or an HIV inhibiting agent. Furthermore, the antitumor activity of the LT-?/LT-? complex may be delivered to tumor cells by tumor infiltrating lymphocytes (TILs) transfected with the gene for LT-?.Type: GrantFiled: November 7, 2001Date of Patent: April 18, 2006Assignees: Biogen, Inc., University of CaliforniaInventors: Jeffrey Browning, Carl F. Ware
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Publication number: 20030143210Abstract: This invention relates to lymphotoxin-&bgr;, a lymphocyte membrane type protein. This protein is found on the surface of a number of cells, including phorbol ester (PMA) stimulated T cell hybridoma II-23.D7 cells. This invention also relates to complexes formed between lymphotoxin-&bgr; and other peptides such as lymphotoxin-&agr; and to complexes comprising multiple subunits of lymphotoxin-&bgr;. These proteins and complexes are useful in holding LT-&agr; formed within the cell on the cell surface where the LT-&agr;/LT-&bgr; complex may act as an inflammation regulating agent, a tumor growth inhibiting agent, a T cell inhibiting agent, a T cell activating agent, an autoimmune disease regulating agent, or an HIV inhibiting agent. Furthermore, the antitumor activity of the LT-&agr;/LT-&bgr; complex may be delivered to tumor cells by tumor infiltrating lymphocytes (TILs) transfected with the gene for LT-&bgr;.Type: ApplicationFiled: November 7, 2001Publication date: July 31, 2003Inventors: Jeffrey L. Browning, Carl F. Ware
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Patent number: 5795964Abstract: This invention relates to lymphotoxin-.beta., a lymphocyte membrane type protein. This protein is found on the surface of a number of cells, including phorbol ester (PMA) stimulated T cell hybridoma II-23.D7 cells. This invention also relates to complexes formed between lymphotoxin-.beta. and other peptides such as lymphotoxin-.alpha. and to complexes comprising multiple subunits of lymphotoxin-.beta.. These proteins and complexes are useful in holding LT-.alpha. formed within the cell on the cell surface where the LT-.alpha./LT-.beta. complex may act as an inflammation regulating agent, a tumor growth inhibiting agent, a T cell inhibiting agent, a T cell activating agent, an autoimmune disease regulating agent, or an HIV inhibiting agent. Furthermore, the antitumor activity of the LT-.alpha./LT-.beta. complex may be delivered to tumor cells by tumor infiltrating lymphocytes (TILs) transfected with the gene for LT-.beta..Type: GrantFiled: June 6, 1995Date of Patent: August 18, 1998Assignees: Biogen, Inc., University of CaliforniaInventors: Jeffrey Browning, Carl F. Ware
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Patent number: 5670149Abstract: This invention relates to lymphotoxin-.beta., a lymphocyte membrane type protein. This protein is found on the surface of a number of cells, including phorbol ester (PNA) stimulated T cell hybridoma II-23.D7 cells. This invention also relates to complexes formed between lymphotoxin-.beta. and other peptides such as lymphotoxin-.alpha. and to complexes comprising multiple subunits of lymphotoxin-.beta.. These proteins and complexes are useful in holding LT-.alpha. formed within the cell on the cell surface where the LT-.alpha./LT-.beta. complex may act as an inflammation regulating agent, a tumor growth inhibiting agent, a T cell inhibiting agent, a T cell activating agent, an autoimmune disease regulating agent, or an HIV inhibiting agent. Furthermore, the antitumor activity of the LT-.alpha./LT-.beta. complex may be delivered to tumor cells by tumor infiltrating lymphocytes (TILs) transfected with the gene for LT-.beta..Type: GrantFiled: June 6, 1995Date of Patent: September 23, 1997Assignees: Biogen, Inc., The University of CaliforniaInventors: Jeffrey Browning, Carl F. Ware