Zusammenfassung
The pathogenesis of rheumatoid arthritis (RA), the most common rheumatic disease, is still an unsolved puzzle. For many years, T-cells were the main focus of research, but recently, the B-cell drew more and more attention not least, due to the observation in humans that the anti-CD20 antibody Retuximab (R), which selectively depletes subsets of B-cells, lessens disease symptoms. A second novel ...
Zusammenfassung
The pathogenesis of rheumatoid arthritis (RA), the most common rheumatic disease, is still an unsolved puzzle. For many years, T-cells were the main focus of research, but recently, the B-cell drew more and more attention not least, due to the observation in humans that the anti-CD20 antibody Retuximab (R), which selectively depletes subsets of B-cells, lessens disease symptoms. A second novel approach to understand pathomechanisms that contribute to the development and progression of arthritis focuses on the sympathetic nervous system, which is known to moderate the function of immune cells, e. g., the B-cell, and therefore, is tied into a complex neuroimmune network that influences the course of the disease. This review first discusses current research that shows the significance of B-cells in the pathogenesis of RA. It then gives a short review of knowledge regarding the role of the sympathetic nervous system (1) in RA pathogenesis and (2) in modulating B-cell responses. Finally, the hypothesis is introduced that the sympathetic nervous system via modulating B-cell function, e. g., antibody production, influences the development and progression of RA.
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