Source:http://linkedlifedata.com/resource/pubmed/id/20215643
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
18
|
| pubmed:dateCreated |
2010-5-7
|
| pubmed:abstractText |
T cells contribute to the pathophysiology of ischemic stroke by yet unknown mechanisms. Mice with transgenic T-cell receptors (TCRs) and mutations in costimulatory molecules were used to define the minimal immunologic requirements for T cell-mediated ischemic brain damage. Stroke was induced in recombination activating gene 1-deficient (RAG1(-/-)) mice devoid of T and B cells, RAG1(-/-) mice reconstituted with B cells or T cells, TCR-transgenic mice bearing 1 single CD8(+) (2C/RAG2, OTI/RAG1 mice) or CD4(+) (OTII/RAG1, 2D2/RAG1 mice) TCR, mice lacking accessory molecules of TCR stimulation (CD28(-/-), PD1(-/-), B7-H1(-/-) mice), or mice deficient in nonclassical T cells (natural killer T [NKT] and gammadelta T cells) by transient middle cerebral artery occlusion (tMCAO). Stroke outcome was assessed at day 1. RAG1(-/-) mice and RAG1(-/-) mice reconstituted with B cells developed significantly smaller brain infarctions compared with controls, but thrombus formation after FeCl(3)-induced vessel injury was unimpaired. In contrast, TCR-transgenic mice and mice lacking costimulatory TCR signals were fully susceptible to tMCAO similar to mice lacking NKT and gammadelta T cells. These findings were corroborated by adoptive transfer experiments. Our data demonstrate that T cells critically contribute to cerebral ischemia, but their detrimental effect neither depends on antigen recognition nor TCR costimulation or thrombus formation.
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| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
May
|
| pubmed:issn |
1528-0020
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| pubmed:author |
pubmed-author:AustinatMadeleineM,
pubmed-author:DreykluftAngelaA,
pubmed-author:HagedornInaI,
pubmed-author:KleinschnitzChristophC,
pubmed-author:KraftPeterP,
pubmed-author:NieswandtBernhardB,
pubmed-author:SchwabNicholasN,
pubmed-author:SchwarzTobiasT,
pubmed-author:StollGuidoG,
pubmed-author:WiendlHeinzH
|
| pubmed:issnType |
Electronic
|
| pubmed:day |
6
|
| pubmed:volume |
115
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
3835-42
|
| pubmed:meshHeading |
pubmed-meshheading:20215643-Adaptive Immunity,
pubmed-meshheading:20215643-Animals,
pubmed-meshheading:20215643-Antigens, CD1d,
pubmed-meshheading:20215643-Antigens, CD28,
pubmed-meshheading:20215643-Brain Ischemia,
pubmed-meshheading:20215643-Cytotoxicity, Immunologic,
pubmed-meshheading:20215643-Female,
pubmed-meshheading:20215643-Genes, RAG-1,
pubmed-meshheading:20215643-Male,
pubmed-meshheading:20215643-Mice,
pubmed-meshheading:20215643-Mice, Inbred C57BL,
pubmed-meshheading:20215643-Mice, Knockout,
pubmed-meshheading:20215643-Mice, Transgenic,
pubmed-meshheading:20215643-Receptors, Antigen, T-Cell,
pubmed-meshheading:20215643-Receptors, Antigen, T-Cell, gamma-delta,
pubmed-meshheading:20215643-Stroke,
pubmed-meshheading:20215643-T-Lymphocytes,
pubmed-meshheading:20215643-Thrombosis
|
| pubmed:year |
2010
|
| pubmed:articleTitle |
Early detrimental T-cell effects in experimental cerebral ischemia are neither related to adaptive immunity nor thrombus formation.
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| pubmed:affiliation |
Department of Neurology, University of Wuerzburg, D-97080 Wuerzburg, Germany. christoph.kleinschnitz@mail.uni-wuerzburg.de
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|