The Sympathetic Nervous System: A Not So ?sympathetic? Regulator Of Immune Function In Autoimmune Disease- Rheumatoid Arthritis As An Example | 19625
Journal of Clinical & Cellular Immunology
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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
-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.
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.
Denise Bellinger completed her PhD at Indiana State University with research training at Indiana University School of Medicine?s onsite campus, and
postdoctoral training in Psychoneuroimmunology from the University of Rochester School of Medicine. She is an Associate Research Professor in the Department
of Pathology and Human Anatomy at Loma Linda University School of Medicine. She has published over 80 peer reviewed papers, review articles, and book
chapters on various aspects of neural-immune interactions in aging and age-related diseases.
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