Source:http://linkedlifedata.com/resource/pubmed/id/18523310
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
12
|
| pubmed:dateCreated |
2008-6-4
|
| pubmed:abstractText |
To identify basic mechanisms of how infections may induce a neuron-specific autoimmune response, we generated mice expressing OVA as neuronal autoantigen under control of the neuron-specific enolase promoter (NSE-OVA mice). Intracerebral, but not systemic, infection with attenuated Listeria monocytogenes-secreting OVA induced an atactic-paretic neurological syndrome in NSE-OVA mice after bacterial clearance from the brain, whereas wild-type mice remained healthy. Immunization with attenuated Listeria monocytogenes-secreting OVA before intracerebral infection strongly increased the number of intracerebral OVA-specific CD8 T cells aggravating neurological disease. T cell depletion and adoptive transfer experiments identified CD8 T cells as decisive mediators of the autoimmune disease. Importantly, NSE-OVA mice having received OVA-specific TCR transgenic CD8 T cells developed an accelerated, more severe, and extended neurological disease. Adoptively transferred pathogenic CD8 T cells specifically homed to OVA-expressing MHC class I(+) neurons and, corresponding to the clinical symptoms, approximately 30% of neurons in the anterior horn of the spinal cord became apoptotic. Thus, molecular mimicry between a pathogen and neurons can induce a CD8 T cell-mediated neurological disease, with its severity being influenced by the frequency of specific CD8 T cells, and its induction, but not its symptomatic phase, requiring the intracerebral presence of the pathogen.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jun
|
| pubmed:issn |
0022-1767
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
15
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| pubmed:volume |
180
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
8421-33
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| pubmed:dateRevised |
2010-11-18
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| pubmed:meshHeading |
pubmed-meshheading:18523310-Adoptive Transfer,
pubmed-meshheading:18523310-Animals,
pubmed-meshheading:18523310-Autoantigens,
pubmed-meshheading:18523310-Brain Diseases,
pubmed-meshheading:18523310-CD4-Positive T-Lymphocytes,
pubmed-meshheading:18523310-CD8-Positive T-Lymphocytes,
pubmed-meshheading:18523310-Cell Differentiation,
pubmed-meshheading:18523310-Chickens,
pubmed-meshheading:18523310-Humans,
pubmed-meshheading:18523310-Listeria monocytogenes,
pubmed-meshheading:18523310-Listeriosis,
pubmed-meshheading:18523310-Mice,
pubmed-meshheading:18523310-Mice, Inbred C57BL,
pubmed-meshheading:18523310-Mice, Transgenic,
pubmed-meshheading:18523310-Molecular Mimicry,
pubmed-meshheading:18523310-Nervous System Autoimmune Disease, Experimental,
pubmed-meshheading:18523310-Neurons,
pubmed-meshheading:18523310-Ovalbumin,
pubmed-meshheading:18523310-Phosphopyruvate Hydratase,
pubmed-meshheading:18523310-Promoter Regions, Genetic,
pubmed-meshheading:18523310-Rats
|
| pubmed:year |
2008
|
| pubmed:articleTitle |
Molecular mimicry between neurons and an intracerebral pathogen induces a CD8 T cell-mediated autoimmune disease.
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| pubmed:affiliation |
Abteilung für Neuropathologie, Universitätsklinikum Köln, Köln, Germany.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|