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pubmed-article:19879804pubmed:abstractTextNeuroinflammation is a pathological hallmark in Parkinson's disease (PD) and amyotrophic lateral sclerosis (ALS), and is characterized by activated microglia and infiltrating T cells at sites of neuronal injury. In PD and ALS, neurons do not die alone; neuronal injury is non-cell-autonomous and depends on a well-orchestrated dialogue in which neuronally secreted misfolded proteins activate microglia and initiate a self-propagating cycle of neurotoxicity. Diverse populations and phenotypes of CD4(+) T cells crosstalk with microglia, and depending on their activation status, influence this dialogue and promote neuroprotection or neurotoxicity. A greater understanding of the T cell population that mediates these effects, as well as the molecular signals involved should provide targets for neuroprotective immunomodulation to treat these devastating neurodegenerative diseases.lld:pubmed
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pubmed-article:19879804pubmed:authorpubmed-author:AppelStanley...lld:pubmed
pubmed-article:19879804pubmed:authorpubmed-author:BeersDavid...lld:pubmed
pubmed-article:19879804pubmed:authorpubmed-author:HenkelJenny...lld:pubmed
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pubmed-article:19879804pubmed:articleTitleT cell-microglial dialogue in Parkinson's disease and amyotrophic lateral sclerosis: are we listening?lld:pubmed
pubmed-article:19879804pubmed:affiliationDepartment of Neurology, Methodist Neurological Institute, The Methodist Hospital Research Institute, The Methodist Hospital, Houston, TX, USA. sappel@tmhs.org <sappel@tmhs.org>lld:pubmed
pubmed-article:19879804pubmed:publicationTypeJournal Articlelld:pubmed
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pubmed-article:19879804pubmed:publicationTypeResearch Support, N.I.H., Extramurallld:pubmed
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