Source:http://linkedlifedata.com/resource/pubmed/id/19879804
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2010-2-4
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pubmed:abstractText |
Neuroinflammation 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.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
1471-4981
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
31
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
7-17
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pubmed:meshHeading |
pubmed-meshheading:19879804-Amyotrophic Lateral Sclerosis,
pubmed-meshheading:19879804-Animals,
pubmed-meshheading:19879804-Cell Communication,
pubmed-meshheading:19879804-Mice,
pubmed-meshheading:19879804-Microglia,
pubmed-meshheading:19879804-Parkinson Disease,
pubmed-meshheading:19879804-T-Lymphocytes
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pubmed:year |
2010
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pubmed:articleTitle |
T cell-microglial dialogue in Parkinson's disease and amyotrophic lateral sclerosis: are we listening?
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pubmed:affiliation |
Department of Neurology, Methodist Neurological Institute, The Methodist Hospital Research Institute, The Methodist Hospital, Houston, TX, USA. sappel@tmhs.org <sappel@tmhs.org>
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pubmed:publicationType |
Journal Article,
Review,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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