Abstract: There is provided agents for modulation of a chronic inflammatory response wherein the agent modulates the biological activity of tenascin-C. There is also provided methods of identifying agents modulating tenascin-C and chronic inflammation. There are also provided uses of such agents.

Abstract: There is provided agents for modulation of a chronic inflammatory response wherein the agent modulates the biological activity of tenascin-C. There is also provided methods of identifying agents modulating tenascin-C and chronic inflammation. There are also provided uses of such agents.

Abstract: There is provided agents for modulation of a chronic inflammatory response wherein the agent modulates the biological activity of tenascin-C. There is also provided methods of identifying agents modulating tenascin-C and chronic inflammation. There are also provided uses of such agents.

Abstract: There is provided agents for modulation of a chronic inflammatory response wherein the agent modulates the biological activity of tenascin-C. There is also provided methods of identifying agents modulating tenascin-C and chronic inflammation. There are also provided uses of such agents.

Abstract: There is provided agents for modulation of a chronic inflammatory response wherein the agent modulates the biological activity of tenascin-C. There is also provided methods of identifying agents modulating tenascin-C and chronic inflammation. There are also provided uses of such agents.

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 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: The present invention provides a method of increasing the TH1:TH2 ratio of an immune response, containing the step of supplying to an antigen presenting cell (APC) such as a dendritic cell (DC) or precursor cell, an intracellular activator of APC, such as DC, function. The invention also provides a method of treating a patient with or at risk of allergy comprising the step of supplying an intracellular activator of APC, such as DC, function, or an intracellular inducer of NF&kgr;B, to the patient or to an APC, such as a DC, or precursor cell, of the patient.

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: The present invention relates to a method of treating a condition comprising administering a pharmaceutically effective amount of an inhibitor of the Tec family of protein tyrosine kinases (PTKs). The condition is typically associated with cytokine production. Conditions addressed by the invention include sepsis, septic shock, inflammation, rheumatoid arthritis and Crohn's disease. In one embodiment, the condition is induced by zymosan. The invention also provides the use of an inhibitor of a member or members of the Tec family of PTKs in the manufacture of a medicament for use in the treatment of a condition associated with cytokine production and methods for identifying an inhibitor of a member or members of the Tec family of PTKs which is also suitable for use in the treatment of a condition associated with stimulus-induced cytokine production.

Abstract: The present invention relates to an improved in vitro method for infecting cells with a viral vector capable of transporting recombinant nucleic acids into the cells. The method comprises the steps of subjecting the cells to elutriation in a velocity gradient, collecting the cells, contacting the cells with at least one cytokine, and infecting 90% or more of the cells with the viral vector at a multiplicity of infection of 50 to 100.

Abstract: Nucleoside thiotriphosphates carrying .sup.32 P in the gamma-thiophosphate group, prepared by reaction between a nucleoside diphosphate and .sup.32 p labelled thiophosphate salt, are used as thiophosphorylating agents for antibodies that bind to tumour-associated antigens. The labelled thiotriphosphates can be used to introduce a therapeutically useful .sup.32 P atom into an antibody that has been modified by the incorporation into its structute of a peptide region capable of acting as a substrate for a phosphokinase. The resulting labelled antibody can then be used for injection in anti-tumour therapy and has clinical advantages over the corresponding phosphoylated analogue.