Kent State University, USA
Title: The sympathetic nervous system: A not so “sympathetic” regulator of immune function in autoimmune disease- Rheumatoid arthritis as an example
Dianne Lorton completed her PhD in Neurosciences at Indiana State University in affiliation with Indiana University School of Medicine. She completed Post-doctoral training in pharmacology at Duke University and in neuroimmunology at the University of Rochester School of Medicine. She is currently an Assistant Professor at Kent State University in the College of Arts and Sciences. She has published over 70 papers (manuscripts, reviews, and book chapters) on neuroimmunology focusing on sympathetic nervous system regulation of immunity.
Mechanisms that cause autoimmune disease are complex and include interactions with genetic, environmental, immunologic, and neural-endocrine factors. How tolerance is broken and disease onset is initiated remain enigmatic. These events are often separated by many years, suggesting that disease onset requires a triggering event that if understood, could be targeted therapeutically. Physical and psychological stressors are implicated in the development of autoimmune disease, based on several observations. First, severe life stressors are strongly associated with disease onset in up to 80% of patients. Second, the major stress pathways, the sympathetic nervous system (SNS) and hypothalamic –pituitary adrenal (HPA)-axis function to restore immune system homeostasis after immune challenges and regulate immune responses that become pathological in autoimmune diseases. Finally, there is a common “trifecta” of dysregulated immune functions, elevated SNS activity and low HPA-axis responsiveness across most autoimmune diseases. Understanding the immune-to-nervous system and nervous -to immune system cross-talk that leads to this ‘trifecta” is key to understanding autoimmune disease mechanisms. Here, we focus on findings indicating elevated SNS tone and altered nerve to 2-adrenergic receptor signaling to the immune system are pathological events required for triggering autoimmunity using in an animal model of rheumatoid arthritis as an example.
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