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David Fox

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Primary Appointment: Int Med-Rheumatology
PubMed Name: Fox DA
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  Research in Dr. Foxs laboratory is directed at defining and characterizing pathways of human T cell activation, and the role of these pathways in the pathogenesis of autoimmune diseases, especially rheumatoid arthritis. Two principal areas of study include: 1- interactions between synovial fibroblasts and T cells, and 2- regulation of Th17 cells. One approach used has been to generate monoclonal antibodies against T lymphocyte populations from autoimmune lesions, for example, from synovial tissue and synovial fluid derived from patients with rheumatoid arthritis. Antibodies are then screened for preferential reactivity with lesional T cells and for functional effects. Using this approach a number of novel T cell surface markers have been identified. The functional roles for these cell surface structures are under active investigation in the laboratory. Systems have been developed to study interactions between lymphocytes and tissue specific cells found in the joint, especially synovial fibroblasts. New monoclonal antibodies have also been developed against RA synoviocytes to further investigate immunologic functions of these cells. The recently recognized Th17 cell subset is assuming a growing role in the pathogenesis of immune-mediated disorders. Using novel systems that allow in vitro differentiation and maturation of Th17 cells, the mechanisms by which IL-4 and other cytokines regulate the Th17 pathway are being investigated. Collagen-induced arthritis, a mouse model of rheumatoid arthritis, has been used to analyze pathogenesis and regulatory roles of effector CD4 subsets in vivo.