Role of Cutaneous B Cells in Discoid Lupus
Our group is the first to identify memory B cells in the skin of patients with discoid lupus. Several observations suggest that B cells contribute to DLE pathogenesis and do so in a manner independent of antibody production, though the mechanism is unknown. These include 1) the requirement for B cells, but not antibody, to induce skin disease in a murine lupus model, 2) the inability of antibody deposition alone to induce skin disease in DLE, and 3) the resolution of skin disease, including discoid lesions, in systemic lupus with anti-B cell therapy (rituximab) without a corresponding change in autoantibody titers. Given these observations and the well- established contribution of B cells to systemic lupus pathogenesis, we hypothesize that B cells in the skin are effectors of DLE pathogenesis in an antibody-independent manner. Studies to test this hypothesis are ongoing.