Abstract: The invention provides CD27 agonists comprising a first component that is an anti-CD27 antibody, or antigen-binding fragment thereof, linked to a second component comprising one or more cross-linking moieties. At least one of the cross-linking moieties does not bind to an Fc receptor and the CD27 agonist stimulates T cell activity without the need for Fc receptor interaction. The cross-linking molecule(s) can be, for example, an anti-CD27, antibody, or antigen-binding fragment thereof, that can be the same or different than the first component. Alternatively, the cross-linking molecule(s) can be a CD27 ligand or a molecule (e.g., antibody) that binds a molecule on a cell such as a T cell, a tumor cell or a stromal cell. Pharmaceutical compositions comprising the CD27 agonists, and methods of using the CD27 agonists, are also provided.

Abstract: The invention provides chimeric antigen receptors (CARs) that specifically bind to the T-cell immunoglobulin and mucin domain 1 (TIM-1) protein. The invention further relates to modified immune cells, e.g., T or NK cells, comprising such CARs, CAR-encoding nucleic acids, CAR-encoding vectors, and methods of making such compositions. The invention further relates to methods for therapeutic use of these CARs and modified immune cells for the treatment of a condition, disorder, or disease associated with cells expressing TIM-1 (e.g., cancer).

Abstract: The invention provides chimeric antigen receptors (CARs) that specifically bind to the T-cell immunoglobulin and mucin domain 1 (TIM-1) protein. The invention further relates to modified immune cells, e.g., T or NK cells, comprising such CARs, CAR-encoding nucleic acids, CAR-encoding vectors, and methods of making such compositions. The invention further relates to methods for therapeutic use of these CARs and modified immune cells for the treatment of a condition, disorder, or disease associated with cells expressing TIM-1 (e.g., cancer).

Abstract: Isolated monoclonal antibodies which bind to human CD27 and related antibody-based compositions and molecules are disclosed. Also disclosed are therapeutic and diagnostic methods for using the antibodies.

Abstract: Isolated monoclonal antibodies which bind to human CD27 and related antibody-based compositions and molecules are disclosed. Also disclosed are therapeutic and diagnostic methods for using the antibodies.

Abstract: The invention provides chimeric antigen receptors (CARs) that specifically bind to the T-cell immunoglobulin and mucin domain 1 (TIM-1) protein. The invention further relates to modified immune cells, e.g., T or NK cells, comprising such CARs, CAR-encoding nucleic acids, CAR-encoding vectors, and methods of making such compositions. The invention further relates to methods for therapeutic use of these CARs and modified immune cells for the treatment of a condition, disorder, or disease associated with cells expressing TIM-1 (e.g., cancer).

Abstract: The invention provides CD27 agonists comprising a first component that is an anti-CD27 antibody, or antigen-binding fragment thereof, linked to a second component comprising one or more cross-linking moieties. At least one of the cross-linking moieties does not bind to an Fc receptor and the CD27 agonist stimulates T cell activity without the need for Fc receptor interaction. The cross-linking molecule(s) can be, for example, an anti-CD27, antibody, or antigen-binding fragment thereof, that can be the same or different than the first component. Alternatively, the cross-linking molecule(s) can be a CD27 ligand or a molecule (e.g., antibody) that binds a molecule on a cell such as a T cell, a tumor cell or a stromal cell. Pharmaceutical compositions comprising the CD27 agonists, and methods of using the CD27 agonists, are also provided.

Abstract: A method is disclosed for treating nephropathies involving undesired alternative pathway complement activation by administration of a complement inhibitory protein such as soluble complement receptor type I (sCR1).

Abstract: A method is disclosed for treating nephropathies involving undesired alternative pathway complement activation by administration of a complement inhibitory protein such as soluble complement receptor type I (sCR1).

Abstract: A method is disclosed for treating nephropathies involving undesired alternative pathway complement activation by administration of a complement inhibitory protein such as soluble complement receptor type I (sCR1).

Abstract: Isolated monoclonal antibodies which bind to human CD27 and related antibody-based compositions and molecules are disclosed. Also disclosed are therapeutic and diagnostic methods for using the antibodies.

Abstract: Isolated monoclonal antibodies which bind to human CD27 and related antibody-based compositions and molecules are disclosed. Also disclosed are therapeutic and diagnostic methods for using the antibodies.

Abstract: A method is disclosed for treating diseases or disorders of the eye involving undesired neovascularization by administration of a complement inhibitory protein such as soluble complement receptor type I (sCR1). The present invention relates to the direct treatment of macular degeneration, particularly age-related macular degeneration (AMD), by administering a complement inhibitory protein intraocularly or systemically.

Abstract: Isolated monoclonal antibodies which bind to human CD27 and related antibody-based compositions and molecules are disclosed. Also disclosed are therapeutic and diagnostic methods for using the antibodies.

Abstract: A method is disclosed for treating nephropathies involving undesired alternative pathway complement activation by administration of a complement inhibitory protein such as soluble complement receptor type I (sCR1).

Abstract: Isolated monoclonal antibodies which bind to human CD27 and related antibody-based compositions and molecules are disclosed. Also disclosed are therapeutic and diagnostic methods for using the antibodies.

Abstract: A method is disclosed for treating diseases or disorders of the eye involving undesired neovascularization by administration of a complement inhibitory protein such as soluble complement receptor type I (sCR1). The present invention relates to the direct treatment of macular degeneration, particularly age-related macular degeneration (AMD), by administering a complement inhibitory protein intraocularly or systemically.

Abstract: The present invention relates to the C3b/C4b receptor (CR1) gene and its encoded protein. The invention also relates to CR1 nucleic acid sequences and fragments thereof comprising 70 nucleotides and their encoded peptides or proteins comprising 24 amino acids. The invention further provides for the expression of the CR1 protein and fragments thereof. The genes and proteins of the invention have uses in diagnosis and therapy of disorders involving complement activity, and various immune system or inflammatory disorders. In specific embodiments of the present invention detailed in the examples sections infra, the cloning, nucleotide sequence, and deduced amino acid sequence of a full-length CR1 cDNA and fragments thereof are described. The expression of the CR1 protein and fragments thereof is also described. Also described is the expression of a secreted CR1 molecule lacking a transmembrane region.

Abstract: Provided are methods of making preparations of recombinant soluble Complement Receptor type 1 (sCR1) defined with respect to the distribution of sCR1 glycoforms and therapeutic methods using them. The preparations are suitable for treatment of allograft or xenograft rejection, diseases involving inflammation or inappropriate complement activation, and thrombotic or shock state conditions. Preferred methods employ sCR1 glycoforms that are sialylated, have a pI of .ltoreq.5.1, or have a sialic acid: mannose molar ratio of .gtoreq.0.25.

Abstract: The present invention relates to the C3b/C4b receptor (CR1) gene and its encoded protein. The invention further provides for the expression of the CR1 protein and fragments thereof. The genes and proteins of the invention have uses in diagnosis and therapy of disorders involving complement activity, and various immune system or inflammatory disorders. In specific embodiments of the present invention detailed in the examples sections infra, the cloning, nucleotide sequence, and deduced amino acid sequence of a full-length CR1 cDNA and fragments thereof are described. The expression of the CR1 protein and fragments thereof is also described. Also described is the expression of a secreted CR1 molecule lacking a transmembrane region. The secreted CR1 molecule is shown to be useful in reducing damage caused by inflammation and in reducing myocardial infarct size and preventing reperfusion injury.