期刊
JOURNAL OF IMMUNOLOGY
卷 182, 期 7, 页码 4137-4149出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0803982
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资金
- Frances and Louie Blumkin Foundation
- Community Neuroscience: Pride of Nebraska Research Initiative
- Alan Baer Charitable Trust
- University of Nebraska Medical Center Patterson Fellowship
- National Institutes of Health [5P01NS31492, 2R37 NS36126, 2R01 NS034239, P20RR15635, U54NS43011, P01MH64570, P01 NS43985]
Microglial inflammatory neuroregulatory activities affect the tempo of nigrostriatal degeneration during Parkinson's disease (PD). Such activities are induced, in part, by misfolded, nitrated alpha-synuclein (N-alpha-syn) within Lewy bodies released from dying or dead dopaminergic neurons. Such pathobiological events initiate innate and adaptive immune responses affecting neurodegeneration. We posit that the neurobiological activities of activated microglia are affected by cell-protein and cell-cell contacts, in that microglial interactions with N-alpha-syn and CD4(+) T cells substantively alter the microglial proteome. This leads to alterations in cell homeostatic functions and disease. CD4(+)CD25(+) regulatory T cells suppress N-alpha-syn microglial-induced reactive oxygen species and NF-kappa B activation by modulating redox-active enzymes, cell migration, phagocytosis, and bioenergetic protein expression and cell function. In, contrast, CD4(+)CD25(-) effector T cells exacerbate microglial inflammation and induce putative neurotoxic responses. These data support the importance of adaptive immunity in the regulation of Parkinson's disease-associated microglial inflammation. The Journal of Immunology, 2009, 182: 4137-4149.
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