Abstract: The present invention relates to methods of modulating cell migration, particularly, monocyte, neutrophil or macrophage migration, using galectin-3, galectin-3 binding polypeptide, or galectin-3 receptor binding polypeptide. Specifically provided are methods for increasing cell migration to sites of inflammation, infection or a tumor. Also provided are methods for identifying agents that modulate galectin-3 mediated migration, compositions containing galectin-3 or a functional subsequence thereof, and microfabricated devices that deliver galectin-3 or functional galectin-3 subsequences.

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.

Abstract: The invention is directed to human antibodies that bind CD40 (e.g., human CD40), methods of producing the antibodies and methods of use. Invention human CD40 antibodies include antibodies that can modulate one or more activities of CD40, such as increasing or decreasing cell proliferation. Invention human CD40 antibodies are therefore useful for increasing or decreasing a CD40 activity in order to alter CD40 activity in vivo.

Abstract: The present invention relates to novel galectin 11 proteins which are members of the galectin superfamily. In particular, isolated nucleic acid molecules are provided encoding the human galectin 11 proteins. Galectin 11 polypeptides are also provided as are vectors, host cells and recombinant methods for producing the same. The invention further relates to screening methods for identifying agonists and antagonists of galectin 11 activity. Also provided are diagnostic and therapeutic methods.

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.

Abstract: The present invention provides a novel method for the treatment of cellular accumulation in chronic inflammatory diseases such as rheumatoid arthritis. The method includes gene delivery and gene expression that is capable of enhancing apoptosis of accumulating cells and those cells which recruit accumulating cells. Also provided are diagnostic methods for detecting cellular accumulation diseases.

Abstract: The present invention relates to novel galectin 11 proteins which are members of the galectin superfamily. In particular, isolated nucleic acid molecules are provided encoding the human galectin 11 proteins. Galectin 11 polypeptides are also provided as are vectors, host cells and recombinant methods for producing the same. The invention further relates to screening methods for identifying agonists and antagonists of galectin 11 activity. Also provided are diagnostic and therapeutic methods.

Abstract: The present invention relates to galectin 11 proteins which are members of the galectin superfamily. In particular, the present invention relates to full-length polypeptides, fragments, and variants of galectin 11.

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.

Abstract: Polypeptides, polynucleotides, fragments thereof, and monoclonal antibodies thereto are provided for antigen-specific and antigen-non-specific glycosylation inhibiting factor and a method for recombinant production of biologically active polypeptides from a structural gene encoding the polypeptide.

Abstract: Antigen non-specific human glycosylation inhibiting factor derivatives having the inmunosuppressive activity in which a mutation was introduced for replacement, deletion and/or insertion of a part of the amino acid sequence of SEQ ID NO:21, and/or which has received a chemical modification of one or more amino acid residue(s) in the amino acid sequence of SEQ ID NO:21, wherein the mutation and the chemical modification attenuate the strength of an intermolecular association in the region, which participates in trimerization, of an antigen non-specific human glycosylation inhibiting factor having the amino acid sequence of SEQ ID NO:21; DNAs containing a base sequence encoding the amino acid sequence of the antigen non-specific human glycosylation inhibiting factor derivative; recombinant vectors containing the DNAs; prokaryotic or eukaryotic cells transformed with the DNAs; methods of producing the antigen non-specific human glycosylation inhibiting factor derivatives; pharmaceutical compositions comprising t

Abstract: A method for the recombinant production and for the isolation of antigen-specific glycosylation inhibiting factor (AgGIF) is provided. Also disclosed is a method for modulating the immune responses in an antigen-specific manner utilizing a AgGIF, comprising soluble non-specific GIF-TCR.alpha. chains which bind to the antigen, and which suppress the immune response in an antigen-specific fashion.

Abstract: Polypeptides, polynucleotides, fragments thereof, and monoclonal antibodies thereto are provided for antigen-specific and antigen-non-specific glycosylation inhibiting factor and a method for recombinant production of biologically active polypeptides from a structural gene encoding the polypeptide.

Abstract: The present invention provides antigen-specific human glycosylation inhibiting factor (GIF), Hybridoma cell lines ATCC HB 10473 and 11052 are provided as exemplary cell lines which produce human antigen-specific human GIF, directed toward honey bee venom and cedar pollen, respectively.

Abstract: A method is disclosed for enhancement of the efficacy of therapeutic treatment for inducing cell death in a cell having an anti-apoptotic gene by the enhancement of apoptosis. An antisense oligonucleotide is disclosed which hybridizes with the nucleic acid sequence of the anti-apoptotic gene. The oligonucleotide is administered to the cell in an amount sufficient to inhibit expression of the gene, thus rendering the cell susceptible to induction of apoptosis, and consequently achieving higher efficacy of therapeutic treatment.

Abstract: The present invention provides antigen-specific human glycosylation inhibiting factor (GIF) and a method for immunosuppression of a specific immune response. Preferably, the antigen-specific GIF is directed toward an allergen. Hybridoma cell lines, ATCC HB 10472 and 10473, are provided as exemplary cell lines which produce human antigen-specific human glycosylation inhibiting factor directed toward cedar pollen and honey bee venom allergen, respectively.