Source:http://linkedlifedata.com/resource/pubmed/id/18462836
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
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| pubmed:dateCreated |
2009-12-16
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| pubmed:abstractText |
The mechanism of circulating T cells entry into the brain in Alzheimer's diseases (AD) remains unclear. Here, we showed that peripheral T cells derived from AD patients overexpress CXCR2 to enhance its transendothelial migration. T cells migration through in vitro blood-brain barrier model was effectively blocked by anti-CXCR2 antibody or IL-8 (a CXCR2 ligand) RNAi in human brain microvascular endothelial cells (HBMECs). Amyloid beta (Abeta) injection in rat hippocampus upregulated CXCR2 expression accompanied with increased T cells occurrence in the brain, and this enhanced T cells entry was effectively blocked by CXCR2 antagonist. Furthermore, anti-TNF-alpha antibody blocked IL-8 production in HBMECs and T cells transendothelial migration caused by the culture supernatant of microglia treated with Abeta. Blockage of intracerebral TNF-alpha abolished the upregulation of CXCR2 in peripheral T cells and the increased T cells occurrence in the brain induced by Abeta injection in rat hippocampus. These data suggest that CXCR2 overexpression in peripheral T cells is intracerebral microglial TNF-alpha-dependent and TNF-alpha primes T cells transendothelial migration in Alzheimer's diseases.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Amyloid beta-Peptides,
http://linkedlifedata.com/resource/pubmed/chemical/Autoantibodies,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-8,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-8B,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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| pubmed:status |
MEDLINE
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| pubmed:month |
Feb
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| pubmed:issn |
1558-1497
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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 |
175-88
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| pubmed:dateRevised |
2010-11-18
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| pubmed:meshHeading |
pubmed-meshheading:18462836-Aged,
pubmed-meshheading:18462836-Aged, 80 and over,
pubmed-meshheading:18462836-Alzheimer Disease,
pubmed-meshheading:18462836-Amyloid beta-Peptides,
pubmed-meshheading:18462836-Animals,
pubmed-meshheading:18462836-Autoantibodies,
pubmed-meshheading:18462836-Blood-Brain Barrier,
pubmed-meshheading:18462836-Brain,
pubmed-meshheading:18462836-Cell Movement,
pubmed-meshheading:18462836-Endothelium, Vascular,
pubmed-meshheading:18462836-Female,
pubmed-meshheading:18462836-Humans,
pubmed-meshheading:18462836-Interleukin-8,
pubmed-meshheading:18462836-Male,
pubmed-meshheading:18462836-Microglia,
pubmed-meshheading:18462836-Microvessels,
pubmed-meshheading:18462836-Rats,
pubmed-meshheading:18462836-Rats, Wistar,
pubmed-meshheading:18462836-Receptors, Interleukin-8B,
pubmed-meshheading:18462836-T-Lymphocytes,
pubmed-meshheading:18462836-Tumor Necrosis Factor-alpha
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| pubmed:year |
2010
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| pubmed:articleTitle |
Peripheral T cells derived from Alzheimer's disease patients overexpress CXCR2 contributing to its transendothelial migration, which is microglial TNF-alpha-dependent.
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| pubmed:affiliation |
Department of Developmental Biology, Key Laboratory of Cell Biology, Ministry of Public Health of China, China Medical University, Shenyang 110001, PR China.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|