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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
12
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pubmed:dateCreated |
2001-6-6
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pubmed:abstractText |
Encephalitogenic T cells that mediate experimental autoimmune encephalomyelitis (EAE) are commonly assumed to be exclusively CD4+, but formal proof is still lacking. In this study, we report that synthetic peptides 35-55 from myelin oligodendrocyte glycoprotein (pMOG(35-55)) consistently activate a high proportion of CD8+ alphabetaTCR+ T cells that are encephalitogenic in C57BL/6 (B6) mice. The encephalitogenic potential of CD8+ MOG-specific T cells was established by adoptive transfer of CD8-enriched MOG-specific T cells. These cells induced a much more severe and permanent disease than disease actively induced by immunization with pMOG(35-55). CNS lesions in pMOG(35-55) CD8+ T cell-induced EAE were progressive and more destructive. The CD8+ T cells were strongly pathogenic in syngeneic B6 and RAG-1(-/-) mice, but not in isogeneic beta2-microglobulin-deficient mice. MOG-specific CD8+ T cells could be repeatedly reisolated for up to 287 days from recipient B6 or RAG-1(-/-) mice in which disease was induced adoptively with <1 x 10(6) T cells sensitized to pMOG(35-55). It is postulated that MOG induces a relapsing and/or progressive pattern of EAE by eliciting a T cell response dominated by CD8+ autoreactive T cells. Such cells appear to have an enhanced tissue-damaging effect and persist in the animal for long periods.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0022-1767
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
166
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
7579-87
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:11390514-Adoptive Transfer,
pubmed-meshheading:11390514-Amino Acid Sequence,
pubmed-meshheading:11390514-Animals,
pubmed-meshheading:11390514-CD8-Positive T-Lymphocytes,
pubmed-meshheading:11390514-Cell Movement,
pubmed-meshheading:11390514-Central Nervous System,
pubmed-meshheading:11390514-Chronic Disease,
pubmed-meshheading:11390514-DNA Nucleotidyltransferases,
pubmed-meshheading:11390514-Disease Progression,
pubmed-meshheading:11390514-Encephalomyelitis, Autoimmune, Experimental,
pubmed-meshheading:11390514-Epitopes, T-Lymphocyte,
pubmed-meshheading:11390514-Homeodomain Proteins,
pubmed-meshheading:11390514-Injections, Intraperitoneal,
pubmed-meshheading:11390514-Lymphocyte Activation,
pubmed-meshheading:11390514-Macrophages,
pubmed-meshheading:11390514-Mice,
pubmed-meshheading:11390514-Mice, Inbred C57BL,
pubmed-meshheading:11390514-Mice, Knockout,
pubmed-meshheading:11390514-Microglia,
pubmed-meshheading:11390514-Molecular Sequence Data,
pubmed-meshheading:11390514-Myelin Proteins,
pubmed-meshheading:11390514-Myelin-Associated Glycoprotein,
pubmed-meshheading:11390514-Peptide Fragments,
pubmed-meshheading:11390514-Recurrence,
pubmed-meshheading:11390514-VDJ Recombinases,
pubmed-meshheading:11390514-Vaccination
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pubmed:year |
2001
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pubmed:articleTitle |
Myelin antigen-specific CD8+ T cells are encephalitogenic and produce severe disease in C57BL/6 mice.
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pubmed:affiliation |
Department of Neurology, and Division of Clinical Immunology and Rheumatology, University of Alabama, Birmingham, AL 35294, USA. dsun@uab.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
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