Abstract: Methods for treating and/or preventing a TNF-mediated disease in an individual are disclosed. Also disclosed is a composition comprising methotrexate and an anti-tumor necrosis factor antibody. TNF-mediated diseases include rheumatoid arthritis, Crohn's disease, and acute and chronic immune diseases associated with transplantation.

Abstract: Methods for treating and/or preventing a TNF-mediated disease in an individual are disclosed. Also disclosed is a composition comprising methotrexate and an anti-tumor necrosis factor antibody. TNF-mediated diseases include rheumatoid arthritis, Crohn's disease, and acute and chronic immune diseases associated with transplantation.

Abstract: Methods for treating and/or preventing a TNF-mediated disease in an individual are disclosed. Also disclosed is a composition comprising methotrexate and an anti-tumor necrosis factor antibody. TNF-mediated diseases include rheumatoid arthritis, Crohn's disease, and acute and chronic immune diseases associated with transplantation.

Abstract: Methods for treating and/or preventing a TNF-mediated disease in an individual are disclosed. Also disclosed is a composition comprising methotrexate and an anti-tumor necrosis factor antibody. TNF-mediated diseases include rheumatoid arthritis, Crohn's disease, and acute and chronic immune diseases associated with transplantation.

Abstract: Methods for treating and/or preventing a TNF-mediated disease in an individual are disclosed. Also disclosed is a composition comprising methotrexate and an anti-tumor necrosis factor antibody. TNF-mediated diseases include rheumatoid arthritis, Crohn's disease, and acute and chronic immune diseases associated with transplantation.

Abstract: The present invention relates to a receptor molecule which binds to TNF comprising all or a functional portion of the extracellular domain (ECD) of two or more TNF-Rs linked via one or more polypeptide linkers. The receptor can further comprise a signal peptide of a secreted protein, such as the signal peptide of the extracellular domain of the TNF-R or the signal peptide of a cytokine. The invention also relates to isolated DNA encoding a receptor molecule which binds to TNF, comprising two or more sequences encoding all or a functional portion of the ECD of TNF-Rs linked via one or more sequences encoding a polypeptide linker. The invention further relates to a method of making a construct which expresses all or a functional portion of the ECD of two or more TNF-Rs linked via one or more polypeptide linkers and cells which express the construct.

Abstract: Activation of the immune response by NF-kB inducers, induction of an anergic response by NF-kB inhibitors and the inhibition and activation of immune response by the administration of an activator or inhibitor of NF-kB is disclosed. Examples of NF-kB inhibitors include IkB?, PSI, a nucleotide sequence encoding IkB? anti-sense nucleic acid encoding an NF-kB sequence, such as Rel B, and anti-NF-kB antibodies. Examples of NF-kB inducers include NIK, MEKK, IKK2, TFRRF2, and Rel B. Also disclosed are vectors encoding inducers and inhibitors of NF-kB, for example adenoviral vectors.

Abstract: Methods for treating and/or preventing a TNF-mediated disease in an individual are disclosed. Also disclosed is a composition comprising methotrexate and an anti-tumor necrosis factor antibody. TNF-mediated diseases include rheumatoid arthritis, Crohn's disease, and acute and chronic immune diseases associated with transplantation.

Abstract: Methods for treating and/or preventing a TNF-mediated disease in an individual are disclosed. Also disclosed is a composition comprising methotrexate and an anti-tumor necrosis factor antibody. TNF-mediated diseases include rheumatoid arthritis, Crohn's disease, and acute and chronic immune diseases associated with transplantation.

Abstract: Methods for treating and/or preventing a TNF-mediated disease in an individual are disclosed. Also disclosed is a composition comprising methotrexate and an anti-tumor necrosis factor antibody. TNF-mediated diseases include rheumatoid arthritis, Crohn's disease, and acute and chronic immune diseases associated with transplantation.

Abstract: We describe (1) a method of enhancing antigen presentation, comprising the step of supplying to an antigen presenting cell such as a dendritic cell, or precursor cell, an inhibitor of Toll-related receptor (TRR) signalling and (2) a method of inhibiting antigen presentation, comprising the step of supplying to an antigen presenting cell such as a dendritic cell, or precursor cell, an enhancer of Toll-related receptor (TRR) signalling. The inhibitor of TRR signalling may be a dominant negative mutant of MyD88, for example MyD881pr.

Abstract: A method of treating or preventing a cardiovascular and/or a cerebrovascular disorder in an individual is disclosed. Also disclosed is a method for treating and/or preventing a thrombotic disorder in an individual. Further disclosed is a method of decreasing plasma fibrinogen in an individual.

Abstract: A method of treating or preventing a cardiovascular and/or a cerebrovascular disorder in an individual is disclosed. Also disclosed is a method for treating and/or preventing a thrombotic disorder in an individual. Further disclosed is a method of decreasing plasma fibrinogen in an individual.

Abstract: Methods for treating and/or preventing a TNF-mediated disease in an individual are disclosed. Also disclosed is a composition comprising methotrexate and an anti-tumor necrosis factor antibody. TNF-mediated diseases include rheumatoid arthritis, Crohn's disease, and acute and chronic immune diseases associated with transplantation.

Abstract: A method of identifying a compound with efficacy in the treatment of chronic inflammatory disease by testing the compound for an ability to selectively inhibit the ability of Tck cells to induce pro-inflammatory cytokine release from a monocyte is disclosed. The method includes pre-incubatin Tck cells with a compound to be tested, optionally resuspending the Tck cells in the absence of the test compound, co-culturing the Tck cells with monocytes, and assaying for the production of pro-inflammatory cytokines by the monocytes. The Tck cells are produced by incubating a population of T cells with one or more cytokines or the Tck cells are isolated from synovial tissue. The Tck cells have not been contacted with an anti-CD3 antibody. The ability to selectively inhibit cytokine release indicates that the compound has efficacy in the treatment of chronic inflammatory disease.

Abstract: Activation of the immune response by NF-kB inducers, induction of an anergic response by NF-kB inhibitors and the inhibition and activation of immune response by the administration of an activator or inhibitor of NF-kB is disclosed. Examples of NF-kB inhibitors include IkB?, PSI, a nucleotide sequence encoding IkB? anti-sense nucleic acid encoding an NF-kB sequence, such as Rel B, and anti-NF-kB antibodies. Examples of NF-kB inducers include NIK, MEKK, IKK2, TFRRF2, and Rel B. Also disclosed are vectors encoding inducers and inhibitors of NF-kB, for example adenoviral vectors.

Abstract: Methods for treating and/or preventing a TNF-mediated disease in an individual are disclosed. Also disclosed are compositions comprising a TNF antagonist and an IL-12 antagonist. TNF-mediated diseases include rheumatoid arthritis, Crohn's disease, and acute and chronic immune diseases associated with transplantation.

Abstract: The present invention relates to a receptor molecule which binds to TNF comprising all or a functional portion of the extracellular domain (ECD) of two or more TNF-Rs linked via one or more polypeptide linkers. The receptor can further comprise a signal peptide of a secreted protein, such as the signal peptide of the extracellular domain of the TNF-R or the signal peptide of a cytokine. The invention also relates to isolated DNA encoding a receptor molecule which binds to TNF, comprising two or more sequences encoding all or a functional portion of the ECD of TNF-Rs linked via one or more sequences encoding a polypeptide linker. The invention further relates to a method of making a construct which expresses all or a functional portion of the ECD of two or more TNF-Rs linked via one or more polypeptide linkers and cells which express the construct.

Abstract: The present invention relates to a receptor molecule which binds to TNF comprising all or a functional portion of the extracellular domain (ECD) of two or more TNF-Rs linked via one or more polypeptide linkers. The receptor can further comprise a signal peptide of a secreted protein, such as the signal peptide of the extracellular domain of the TNF-R or the signal peptide of a cytokine. The invention also relates to isolated DNA encoding a receptor molecule which binds to TNF, comprising two or more sequences encoding all or a functional portion of the ECD of TNF-Rs linked via one or more sequences encoding a polypeptide linker. The invention further relates to a method of making a construct which expresses all or a functional portion of the ECD of two or more TNF-Rs linked via one or more polypeptide linkers and cells which express the construct.

Abstract: Fusion proteins comprising a Receptor for Advanced Glycation End Products Ligand Binding Element (RAGE-LBE) and an immunoglobulin element are disclosed. Also disclosed are fusion proteins comprising a RAGE-LBE and a dimerization domain. Also disclosed are nucleic acids encoding such fusion proteins and methods for using disclosed nucleic acids and proteins to, for example, treat RAGE-related disorders. Additional compositions and methods are also disclosed.