The role of the sympathetic neuroimmune modulation of the B cell in arthritis

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Rheumatoid arthritis (RA) is the most common rheumatic disease and affects 1% of the population. Recent studies have shown that the sympathetic nervous system (SNS) by release of sympathetic neurotransmitters and subsequent stimulation of receptors on immune cells has a profound effect on the course and development of arthritis. One of those immune cells that is susceptible for signals from the sympathetic nervous system, is the B cell, which has been shown to increase antibody production following stimulation with the sympathetic neurotransmitter norepinephrine in own recent work. On the other hand, B cells also contribute to the pathogenesis of arthritis by several means (antigen presentation, cytokine production, and autoantibody secretion). However, the role of sympathetic neuroimmunomodulation of B cells and its effect on the development and severity of arthritis is not known and will be investigated in this project using isolated human synovial B cells, as well as utilizing an established model of collagen-type II induced arthritis. This project will delineate new possible therapeutic targets at the interface between the SNS and the B cell in arthritis.