ROS Modulation of Innate and Adaptive Immunity in RA

$54,049P30FY2011ARNIH

University Of Alabama At Birmingham, Birmingham AL

Investigators

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Abstract

Rheumatoid arthritis is an autoimmune-mediated chronic inflammatory disease mediated by T cells, macrophages, synoviocytes, fibroblasts, and B cells, and other immune cells that result in the progressive destruction of joints (20-26). Cytokines such as TNF-a, IL-IB, and IL-6 have a vital role in mediating the inflammation and pathogenesis of RA in the synovial membrane (27). A two-prong approach to protect the synovial membrane and joint from this initial damage in RA is to block the production and/or action of ROS and pro-inflammatory cytokines, but also inhibit ROS-dependent signaling pathways in macrophages and T cells that are necessary for pro-inflammatory third signal synthesis and adaptive immune maturation (28-31). Altering redox balance and third signal synthesis with a CA can modulate innate and adaptive immunity to not only nominal antigens (31, 32), but may also be efficacious in autoimmune diseases such as rheumatoid arthritis as we have demonstrated previously with Type 1 diabetes (10). The significance of our research proposal is to assess the efficacy of a novel immunotherapeutic that specifically ablates ROS, redoxdependent signaling, and pro-inflammatory third signal synthesis as It pertains to innate and adaptive immune activation In rheumatoid arthritis.

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