Carl F Ware

US Patent:

6998108, Feb 14, 2006

Filed:

Mar 13, 2000

Appl. No.:

09/524325

Inventors:

Carl E. Ware - Solana Beach CA, US

Assignee:

La Jolla Institute for Allergy and Immunology - San Diego CA

International Classification:

C07K 16/00
C07K 16/28
C12P 21/08
C12N 15/13
A61K 39/395

US Classification:

424 951, 4241301, 4241451, 435320, 435810, 5303871, 5303873, 5303881, 53038823, 5303897

Abstract:

A novel ligand (p30) for herpes virus entry mediator, HVEM, is provided. p30 is useful for modulating immune responses and in inhibiting infection by herpes virus. Methods for treating subjects with lymphoid cell disorders or those having or suspected of having a herpes virus infection, utilizing p30 of the invention, are also provided.

US Patent:

7030080, Apr 18, 2006

Filed:

Nov 7, 2001

Appl. No.:

10/040281

Inventors:

Jeffrey Browning - Brookline MA, US
Carl F. Ware - Riverside CA, US

Assignee:

Biogen, Inc. - Cambridge MA
University of California - Oakland CA

International Classification:

A61K 38/00

US Classification:

514 2, 4241431, 4241341, 514 8

Abstract:

This invention relates to lymphotoxin-β, 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-β and other peptides such as lymphotoxin-α and to complexes comprising multiple subunits of lymphotoxin-β. These proteins and complexes are useful in holding LT-α formed within the cell on the cell surface where the LT-α/LT-β 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-α/LT-β complex may be delivered to tumor cells by tumor infiltrating lymphocytes (TILs) transfected with the gene for LT-β.

US Patent:

7118742, Oct 10, 2006

Filed:

Sep 28, 2001

Appl. No.:

09/967604

Inventors:

Carl Ware - Solana Beach CA, US

Assignee:

La Jolla Institute for Allergy and Immunology - La Jolla CA

International Classification:

A61K 39/395
A61K 45/00
C07K 16/28
C12P 21/08

US Classification:

4241301, 4241331, 4241431, 424 854, 5303871, 5303873, 5303882

Abstract:

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.

US Patent:

7575745, Aug 18, 2009

Filed:

Aug 29, 2006

Appl. No.:

11/513290

Inventors:

Carl F. Ware - Solana Beach CA, US

Assignee:

La Jolla Institute for Allergy and Immunology - La Jolla CA

International Classification:

A61K 39/395
C07K 14/47
C07K 16/18

US Classification:

4241301, 4241451, 530350, 5303892, 530412, 530413

Abstract:

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.

US Patent:

8058402, Nov 15, 2011

Filed:

Aug 24, 2007

Appl. No.:

12/439518

Inventors:

Steven W. Granger - Encinitas CA, US
Shinichiro Kato - Chiba, JP
Carl F. Ware - Solana Beach CA, US

Assignee:

Kyowa Hakko Kirin - Tokyo
La Jolla Institute for Allergy and Immunology - La Jolla CA

International Classification:

C12P 21/08

US Classification:

5303873, 5303881, 53038815

Abstract:

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. , the hLIGHT-mediated production or secretion of CCL20, IL-8 or RANTES from a cell expressing a hLIGHT receptor).

US Patent:

8153123, Apr 10, 2012

Filed:

Jun 11, 2009

Appl. No.:

12/483159

Inventors:

Carl F. Ware - Solana Beach CA, US
Carl De Trez - Brussels, BE

Assignee:

La Jolla Institute for Allergy and Immunology - La Jolla CA

International Classification:

A61K 39/395

US Classification:

4241301

Abstract:

The present invention provides methods for restoring and increasing dendritic cell populations in a subject by modulation of the lymphotoxin-β receptor (LTβR) via LTβR 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 LTβR agonist.

US Patent:

8349320, Jan 8, 2013

Filed:

Jun 10, 2009

Appl. No.:

12/482426

Inventors:

Carl F. Ware - Solana Beach CA, US
Carl De Trez - Brussels, BE
Michael Croft - San Diego CA, US
Timothy C. Cheung - Sydney, AU
Ian R. Humphreys - St. Brides Major, GB
Karen G. Potter - San Diego CA, US
Christopher A. Benedict - Encinitas CA, US
Mitchell Kronenberg - Del Mar CA, US
Marcos W. Steinberg - San Diego CA, US

Assignee:

La Jolla Institute for Allergy and Immunology - La Jolla CA

International Classification:

A61K 39/395

US Classification:

4241301

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.

US Patent:

8461307, Jun 11, 2013

Filed:

Sep 22, 2011

Appl. No.:

13/240356

Inventors:

Steven W. Granger - Encinitas CA, US
Shinichiro Kato - Chiba CA, US
Carl F. Ware - Solana Beach CA, US

Assignee:

Kyowa Hakko Kirin Co., Limited - Tokyo
La Jolla Institute for Allergy and Immunology - La Jolla CA

International Classification:

C12P 21/08

US Classification:

5303873, 5303881, 53038815

Abstract:

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.