Abstract: Arginine-containing cysteine-modifying compounds useful for MALDI-MS analysis of proteins are provided. These compounds termed isotope-coded ionization enhancement reagents (ICIER) can provide ionization enhancement in MALDI-MS, relative quantitation, and additional database searching constraints at the same time without any extra sample manipulation. More specifically, ICIER increase the ionization efficiency of cysteine-containing peptides by attachment of a guanidino functional group. ICIER also increase the overall hydrophilicity of these peptides due to the hydrophilic nature of ICIER and thus increase the percentage of recovery of these peptides during sample handling and processing such as in-gel digestion or liquid chromatography.
Type:
Grant
Filed:
October 22, 2001
Date of Patent:
June 14, 2005
Assignee:
Genetics Institute, Inc.
Inventors:
Yongchang Qiu, Jack H. Wang, Rodney M. Hewick
Abstract: Methods for inducing a population of T cells to proliferate by activating the population of T cells and stimulating an accessory molecule on the surface of the T cells with a ligand which binds the accessory molecule are described. T cell proliferation occurs in the absence of exogenous growth factors or accessory cells. T cell activation is accomplished by stimulating the T cell receptor (TCR)/CD3 complex or the CD2 surface protein. To induce proliferation of an activated population T cells, an accessory molecule on the surface of the T cells, such as CD28, is stimulated with a ligand which binds the accessory molecule. The T cell population expanded by the method of the invention can be genetically transduced and used for immunotherapy or can be used in methods of diagnosis.
Type:
Grant
Filed:
July 8, 1999
Date of Patent:
June 14, 2005
Assignees:
Genetics Institute, Inc., Regents of the University of Michigan, The United States of America as represented by the Secretary of the Navy
Inventors:
Carl H. June, Craig B. Thompson, Gary J. Nabel, Gary S. Gray, Paul D. Rennert
Abstract: Methods for inducing a population of T cells to proliferate by activating the population of T cells and stimulating an accessory molecule on the surface of the T cells with a ligand which binds the accessory molecule are described. T cell proliferation occurs in the absence of exogenous growth factors or accessory cells. T cell activation is accomplished by stimulating the T cell receptor (TCR)/CD3 complex or the CD2 surface protein. To induce proliferation of an activated population T cells, an accessory molecule on the surface of the T cells, such as CD28, is stimulated with a ligand which binds the accessory molecule. The T cell population expanded by the method of the invention can be genetically transduced and used for immunotherapy or can be used in methods of diagnosis.
Type:
Grant
Filed:
January 26, 1996
Date of Patent:
June 14, 2005
Assignees:
Genetics Institute, Inc., Regents of the University of Michigan, The United States of America as represented by the Secretary of the Navy
Inventors:
Carl H. June, Craig B. Thompson, Gary J. Nabel, Gary S. Gray, Paul D. Rennert
Abstract: Polynucleotides encoding human CTLA-8 (now known as IL-17F) and related proteins are disclosed. Human CTLA-8 and related proteins, including anti-human IL-17F antibodies, and methods for their production are also disclosed. Methods of treatment using human CTLA-8 proteins, rat CTLA-8 proteins and herpes CTLA-8 proteins are also provided.
Type:
Grant
Filed:
March 19, 2002
Date of Patent:
June 7, 2005
Assignee:
Genetics Institute, LLC
Inventors:
Kenneth Jacobs, Kerry Kelleher, McKeough Carlin, Samuel Goldman, Debra Pittman, Sha Mi, Steven Neben, Joanne Giannotti, Margaret M. Golden-Fleet
Abstract: Antibodies to IL-1-R intracellular ligand proteins are disclosed. The antibodies arc useful for inhibiting the binding between IL-1-R and IL-1-R intracellular ligand proteins.
Abstract: Polynucleotides encoding DADD protein are also disclosed, along with vectors, host cells, and methods of making DADD protein. Methods of identifying inhibitors of DADD death domain binding and inhibitors identified by such methods are also disclosed.
Abstract: Methods for inducing a population of T cells to proliferate by activating the population of T cells and stimulating an accessory molecule on the surface of the T cells with a ligand which binds the accessory molecule are described. T cell proliferation occurs in the absence of exogenous growth factors or accessory cells. T cell activation is accomplished by stimulating the T cell receptor (TCR)/CD3 complex or the CD2 surface protein. To induce proliferation of an activated population T cells, an accessory molecule on the surface of the T cells, such as CD28, is stimulated with a ligand which binds the accessory molecule. The T cell population expanded by the method of the invention can be genetically transduced and used for immunotherapy or can be used in methods of diagnosis.
Type:
Grant
Filed:
July 8, 1999
Date of Patent:
May 3, 2005
Assignees:
Genetics Institute, Inc., Regents of the University of Michigan, The United States of America as represented by the Secretary of the Navy
Inventors:
Carl H. June, Craig B. Thompson, Gary J. Nabel, Gary S. Gray, Paul D. Rennert
Abstract: Highly purified mocarhagin, a cobra venom protease, is disclosed. Pharmaceutical compositions and therapeutic uses of the highly purified protease are also provided. Polynucleotides encoding such protease and related proteases are also disclosed.
Type:
Grant
Filed:
November 27, 2001
Date of Patent:
April 19, 2005
Assignee:
Genetics Institute, LLC
Inventors:
Amechand Boodhoo, Jasbir S. Seehra, Gray Shaw, Dianne Sako
Abstract: Method of treating autoimmune conditions are disclosed comprising administering to a mammalian subject IL-12 or an IL-12 antagonist. In certain preferred embodiments the autoimmune condition is one which is promoted by an increase in levels of IFN-? or TNF-?. Suitable conditions for treatment include multiple sclerosis, systemic lupus erythematosus, rheumatoid arthritis, autoimmune pulmonary inflammation, Guillain-Barre syndrome, autoimmune thyroiditis, insulin dependent diabetes melitis and autoimmune inflammatory eye disease.
Type:
Application
Filed:
September 11, 2003
Publication date:
April 14, 2005
Applicant:
Genetics Institute, LLC
Inventors:
John Leonard, Samuel Goldman, Richard O'Hara
Abstract: Antibodies and antigen-binding fragments thereof that bind interleukin-22 (IL-22), in particular, human IL-22, and their uses in regulating IL-22-associated immune responses are disclosed. The antibodies disclosed herein are useful in diagnosing, preventing, or treating IL-22-associated immune disorders, e.g., autoimmune disorders (e.g., arthritis).
Abstract: The invention provides a novel calcium-independent cytosolic phospholipase A2-Beta enzyme, polynucleotides encoding such enzyme and methods for screening unknown compounds for anti-inflammatory activity mediated by the arachidonic acid cascade.
Abstract: The invention provides isolated nucleic acids molecules, designated SLIC-1 nucleic acid molecules, which encode novel P-selectin glycoprotein ligand (PSGL-1) binding molecules. The invention also provides antisense nucleic acid molecules, recombinant expression vectors containing SLIC-1 nucleic acid molecules, host cells into which the expression vectors have been introduced, and nonhuman transgenic animals in which a SLIC-1 gene has been introduced or disrupted. The invention still further provides isolated SLIC-1 proteins, fusion proteins, antigenic peptides and anti-SLIC-1 antibodies. Diagnostic methods utilizing compositions of the invention are also provided.
Type:
Grant
Filed:
March 23, 2001
Date of Patent:
February 8, 2005
Assignee:
Genetics Institute, LLC
Inventors:
Meike Lorenz, Ron Kriz, Nadine Weich, Gray D. Shaw
Abstract: Method of treating autoimmune conditions are disclosed comprising administering to a mammalian subject IL-12 or an IL-12 antagonist. In certain preferred embodiments the autoimmune condition is one which is promoted by an increase in levels of IFN-&ggr; or TNF-&agr;. Suitable conditions for treatment include multiple sclerosis, systemic lupus erythematosus, rheumatoid arthritis, autoimmune pulmonary inflammation, Guillain-Barre syndrome, autoimmune thyroiditis, insulin dependent diabetes melitis and autoimmune inflammatory eye disease.
Type:
Grant
Filed:
February 25, 2000
Date of Patent:
December 14, 2004
Assignee:
Genetics Institute, LLC
Inventors:
John Leonard, Samuel Goldman, Richard O'Hara, Jr.
Abstract: The invention relates to a humanized anti-B7-2 antibody that comprises a variable region of nonhuman origin and at least a portion of an immunoglobulin of human origin. The invention also pertains to methods of treatment for various autoimmune diseases, transplant rejection, inflammatory disorders and infectious diseases by administering humanized anti-B7-2 and/or anti-B7-1 antibodies.
Type:
Grant
Filed:
July 27, 2000
Date of Patent:
December 7, 2004
Assignee:
Genetics Institute, LLC
Inventors:
Man Sung Co, Maximiliano Vasquez, Beatriz Carreno, Abbie Cheryl Celniker, Mary Collins, Samuel Goldman, Andrea Knight, Denise O'Hara, Bonita Rup, Geertruida M. Veldman, Gary S. Gray
Abstract: Novel compounds are disclosed which inhibit the activity of phospholipase enzymes, particularly cytosolic phospholipase A2. Pharmaceutical compositions comprising such compounds and methods of treatment using such compositions are also disclosed.
Type:
Grant
Filed:
September 29, 2000
Date of Patent:
December 7, 2004
Assignee:
Genetics Institute, LLC
Inventors:
Jasbir S. Seehra, Neelu Kaila, John McKew, Frank Lovering, Jean E. Bemis, YiBin Xiang
Abstract: The present invention relates to, inter alia, methods for inhibiting the interaction of the B-lymphocyte antigen, B7-2, with its natural ligand on the surface of an immune cell are disclosed. The methods comprise contacting the immune cell with an agent which inhibits B7-2 binding with its natural ligand, to thereby inhibit the interaction. Examples of such agents are provided, and include a soluble form of B7-2, an antibody that recognized B7-2. The method may also include contacting the immune cell with an agent that blocks the interaction of B7-1 with its natural ligand. Further, the method may include contacting the immune cell with an immunomodulating agent, for example, an antibody reactive with CD28, an antibody reactive with CTLA4, an antibody reactive with a cytokine, a CTLA4Ig fusion protein, a CD28Ig fusion protein, and an immunosuppressive drug. Both in vivo and in vitro applications of the method are disclosed.
Type:
Grant
Filed:
October 22, 1999
Date of Patent:
November 30, 2004
Assignees:
Dana-Farber Cancer Institute, Inc., Genetics Institute, LLC
Inventors:
Gordon J. Freeman, Lee M. Nadler, Gary S. Gray
Abstract: The invention identifies PD-1 as a receptor for B7-4. B7-4 can inhibit immune cell activation upon binding to an inhibitory receptor on an immune cell. Accordingly, the invention provides agents for modulating PD-1, B7-4, and the interaction between B7-4 and PD-1 in order to modulate a costimulatory or an inhibitory signal in a immune cell resulting in modulation of the immune response.
Type:
Grant
Filed:
August 23, 2000
Date of Patent:
October 26, 2004
Assignees:
Genetics Institute, Inc., Dana-Farber Cancer Institute, Inc.