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“Taming the Flame” in Autoimmune Arthritis: Reining in Sympathetic Nerve Activity Improves Disease Outcome and Shifts Pro/Anti‐inflammatory Cytokine Balance Uniquely in Relevant Immune Organs

A myriad of factors conspire to obscure the etiology of autoimmunity, such as cytokines, hormones, neurotransmitters, environment and genetics. Thus, the trigger of disease onset remains perplexing. Since up to 80% of patients experience severe life stressors prior to the onset of an autoimmune disease in retrospective studies, including rheumatoid arthritis (RA), physical, and psychological stressors are strongly implicated in triggering the onset of disease. Moreover, autoimmunity itself creates significant stress in patients, providing a possible role for pathways that mediate physiologic responses to stressors in driving disease onset and progression. Still, evidence‐based research remains limited to support this hypothesis. To narrow this gap, we examined the role of high sympathetic nerve activity in the onset of RA using the adjuvant‐induced (AA) arthritis in Lewis rats as a model. We tested the hypothesis that lower sympathetic nerve activity (tone) after disease onset will ameliorate disease and shift inflammatory cytokines toward an anti‐inflammatory profile in relevant immune organs.