Abstract: The disclosure provides a non-naturally occurring BAFF-R glycoprotein having a deletion in the extracellular domain which results in an altered 0-linked glycosylation pattern. The disclosure also provides methods and pharmaceutical compositions for treating B-cell- and T-cell-mediated disorders.

Abstract: The instant invention describes methods of separating or preferentially synthesizing dimers which are linked via at least one interchain disulfide linkage from dimers which are not linked via at least one interchain disulfide linkage from a mixture comprising the two types of polypeptide dimers. These forms can be separated from each other using hydrophobic interaction chromatography. In addition, the invention pertains to connecting peptides that result in the preferential biosynthesis of dimers that are linked via at least one interchain disulfide linkage or that are not linked via at least one interchain disulfide linkage. The invention also pertains to compositions in which a majority of the dimers are linked via at least one interchain disulfide linkage or are not linked via at least one interchain disulfide linkage. The invention still further pertains to novel binding molecules, e.g., comprising connecting peptides of the invention.

Abstract: The present invention is based, at least in part, on the discovery that strategic modifications of non-human donor antibody CDR residue(s) can be used to humanize antibodies. Such modifications modulate the 3D structural fit between donor antibody CDRs and human acceptor antibody framework regions that comprise the variable domains of a CDR-grafted antibody. Whereas prior art methods of humanization have relied on making framework substitutions (in which selected human framework residues are backmutated to the corresponding amino acid residue present in the non-human donor antibody), the instant invention is based, at least in part, on a method of humanizing antibodies in which selected CDR residues, and optionally adjacent FR residues, are changed in order to accommodate differences in FR amino acid sequences between donor and acceptor antibodies.

Abstract: Nucleic acids that encode Tumor Necrosis Factor Related Ligand (TRELL), a novel member of the tumor necrosis factor family (TNF), modified TRELL, are described.

Abstract: Disclosed are antibodies that inhibit proteolytic release of a soluble KIM-1 polypeptide from KIM-1 expressing cells. Also disclosed are methods of using the antibodies to inhibit shedding of the KIM-1 polypeptide.

Abstract: Monoclonal antibodies which specifically bind human CD23, the low affinity receptor for IgE (FceRII/CD23), and contain either a human gamma-1 or human gamma-3 constant domain, are disclosed. The antibodies are useful for modulating or inhibiting induced IgE expression. Accordingly, they have practical utility in the treatment or prophylaxis of disease conditions wherein inhibition of induced IgE production is therapeutically desirable, including allergic conditions, autoimmune diseases and inflammatory diseases.

Abstract: Compounds of formula I possess unexpectedly high affinity for Alk 5 and/or Alk 4, and can be useful as antagonists thereof for preventing and/or treating numerous diseases, including fibrotic disorders.

Abstract: A novel receptor in the TNF family is provided: BAFF-R. Chimeric molecules and antibodies to BAFF-R and methods of use thereof are also provided.

Abstract: Chronic Lymphocytic Leukemia (CLL) may be treated with antibodies directed against the CD20 antigen.

Abstract: The use of KIM-1 antagonists to inhibit signaling between a T cell and a second cell, e.g., an antigen-presenting cell, is disclosed. Such inhibition is useful for treatment of diseases including various autoimmune diseases and graft-versus-host disease. Also disclosed is the use of a KIM-1 antagonist to inhibit secretion of IFN-? by lymphocytes or other immune cells in a mammal. Inhibition of IFN-? is useful for treatment of inflammatory diseases or disorders, e.g., inflammatory bowel disease.

Abstract: Chronic Lymphocytic Leukemia (CLL) may be treated with antibodies directed against the CD20 antigen.

Abstract: The present invention is based, at least in part, on the discovery that strategic modifications of non-human donor antibody CDR residue(s) can be used to humanize antibodies. Such modifications modulate the 3D structural fit between donor antibody CDRs and human acceptor antibody framework regions that comprise the variable domains of a CDR-grafted antibody. Whereas prior art methods of humanization have relied on making framework substitutions (in which selected human framework residues are backmutated to the corresponding amino acid residue present in the non-human donor antibody), the instant invention is based, at least in part, on a method of humanizing antibodies in which selected CDR residues, and optionally adjacent FR residues, are changed in order to accommodate differences in FR amino acid sequences between donor and acceptor antibodies.

Abstract: Biomarkers useful for identifying treatments for and monitoring treatment of patients with multiple sclerosis (MS) are provided, as well as methods for their identification, methods of diagnosing MS, relapse of MS patients and disease progression in MS patients.

Abstract: The invention is based on the discovery that compounds of formula (I) possess unexpectedly high affinity for the A2a adenosine receptor, and can be useful as antagonists thereof for preventing and/or treating numerous diseases, including Parkinson's disease.

Abstract: The invention provides Cripto blocking antibodies, or biologically functional fragments thereof, and uses thereof. Antibodies which bind Cripto and modulate Cripto signaling are provided. Antibodies which bind Cripto and block the interaction between Cripto and ALK4 are provided. Antibodies which bind Cripto and modulate tumor growth are also provided. Antibodies which bind Cripto, modulate signaling, and modulate tumor growth are also provided. Antibodies which bind Cripto, block the interaction between Cripto and ALK4 and modulate tumor growth are provided. The invention also provides methods of using these antibodies in therapeutic, diagnostic, and research applications.

Abstract: Disclosed are methods of increasing serum exposure of an administered glial cell line-derived neurotrophic factor (GDNF) ligand family protein by administering to a subject via systemic delivery (i) a GDNF ligand family protein, and (ii) an amount of heparin or heparan sulphate that increases serum exposure of the administered GDNF ligand family protein in the subject.

Abstract: The present invention is based, at least in part, on the discovery that the pseudogene TDGF3 (Cripto-3) is expressed in cells and, in particular, that TDGF3 overexpression is associated with transformation of a cell, e.g., TDGF3 is overexpressed in cancer cell lines and cells from tumor tissue. Accordingly, the invention provides compositions, kits, and methods for detecting the presence of a TDGF3 polynucleotide or polypeptide in a sample. The invention further provides compositions, kits and methods for assessing whether a cell is transformed as well as for assessing whether a patient is a suitable candidate for an anti-Cripto antibody therapy.

Abstract: In one aspect, the invention features a compound of the general Formula (I). Compounds of Formula (I) possess high affinity for Alk 5 and/or AIk 4, and can be useful as antagonists thereof for preventing and/or treating numerous diseases, including fibrotic disorders.

Abstract: The invention relates to neublastin neurotrophic factor polypeptides, nucleic acids encoding neublastin polypeptides, and antibodies that bind specifically to neublastin polypeptides, as well as methods of making and methods of using the same.

Abstract: The present application describes methods for blocking immune response to foreign antigens in a mammal using antagonists which bind to CD20.