Innate and Adaptive Immunity for the Pathobiology of Parkinson's Disease

被引:1
作者
Stone, David K. [1 ]
Reynolds, Ashley D. [1 ]
Mosley, R. Lee [1 ]
Gendelman, Howard E. [1 ]
机构
[1] Univ Nebraska, Med Ctr, Ctr Neurovirol & Neurodegenerat Disorders, Dept Pharmacol & Expt Neurosci, Omaha, NE USA
关键词
REGULATORY T-CELLS; NONSTEROIDAL ANTIINFLAMMATORY DRUGS; VASOACTIVE-INTESTINAL-PEPTIDE; CENTRAL-NERVOUS-SYSTEM; TRANSCRIPTION FACTOR FOXP3; MEDIAL FOREBRAIN-BUNDLE; EXPERIMENTAL AUTOIMMUNE-THYROIDITIS; SYNUCLEIN ACTIVATES MICROGLIA; STRIATAL DOPAMINERGIC-NEURONS; COLONY-STIMULATING FACTOR;
D O I
10.1089/ars.2009.2460
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Innate and adaptive immunity affect the pathogenesis of Parkinson's disease (PD). In particular, activation of microglia influences degeneration of dopaminergic neurons. Cell-to-cell interactions and immune regulation critical for neuronal homeostasis also influence immune responses. The links between T cell immunity and nigrostriatal degeneration are supported by laboratory, animal model, and human pathologic investigations. Immune-associated biomarkers in spinal fluids and brain tissue of patients with idiopathic or familial forms of PD provide means to improve diagnosis and therapeutic monitoring. Relationships between oxidative stress, inflammation, and immune-mediated cell death pathways are examined in this review as they are linked to PD pathogenesis. Harnessing the immune system by drugs or by vaccination remain promising future therapeutic options. Antioxid. Redox Signal. 11, 2151-2166.
引用
收藏
页码:2151 / 2166
页数:16
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