The Role of Innate and Adaptive Immunity in Parkinson's Disease

• Type of Material: Article
• Authors: George T. Kannarkat, Emory University; Jeremy Boss, Emory University; Malu Tansey, Emory University
• Language: English
• Date: 2013-01-01
• Publisher: IOS Press
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2013 -IOS Press and the authors.
• Final Published Version (URL): http://dx.doi.org/10.3233/JPD-130250
• Title of Journal or Parent Work: Journal of Parkinson's Disease
• ISSN: 1877-7171
• Volume: 3
• Issue: 4
• Start Page: 493
• End Page: 514
• Grant/Funding Information: Financial support for the authors of this review includes grants from The Michael J. Fox Foundation for Parkinson's Research Target Validation program (JMB), NIH/NINDS R01NS072467-04 (MGT), NIH/NINDS F31 NS081830-01 (GTK) and NIH/NIGMS RO1 GM47310-16 (JMB).
• Keywords: Parkinson's disease; MEMORY B-CELLS; Immune system; immunomodulation; Neurosciences; adaptive immunity; Life Sciences & Biomedicine; Neurosciences & Neurology; PROTECTS DOPAMINERGIC-NEURONS; NECROSIS-FACTOR-ALPHA; lymphocytes; SYNUCLEIN ACTIVATES MICROGLIA; SUBSTANTIA-NIGRA; GENOME-WIDE ASSOCIATION; CENTRAL-NERVOUS-SYSTEM; H5N1 INFLUENZA-VIRUS; MOUSE MODEL; Science & Technology; FC-GAMMA RECEPTORS; inflammation
• Research Categories: Health Sciences, Immunology; Biology, Neuroscience

Abstract

In recent years, inflammation has become implicated as a major pathogenic factor in the onset and progression of Parkinson's disease. Understanding the precise role for inflammation in PD will likely lead to understanding of how sporadic disease arises. In vivo evidence for inflammation in PD includes microglial activation, increased expression of inflammatory genes in the periphery and in the central nervous system (CNS), infiltration of peripheral immune cells into the CNS, and altered composition and phenotype of peripheral immune cells. These findings are recapitulated in various animal models of PD and are reviewed herein. Furthermore, we examine the potential relevance of PD-linked genetic mutations to altered immune function and the extent to which environmental exposures that recapitulate these phenotypes, which may lead to sporadic PD through similar mechanisms. Given the implications of immune system involvement on disease progression, we conclude by reviewing the evidence supporting the potential efficacy of immunomodulatory therapies in PD prevention or treatment. There is a clear need for additional research to clarify the role of immunity and inflammation in this chronic, neurodegenerative disease.