Source:http://linkedlifedata.com/resource/pubmed/id/11017106
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2001-4-2
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pubmed:abstractText |
A central tenet of T cell development postulates that if a developing thymocyte encounters self-antigen, it is induced to die via apoptosis, thereby protecting the organism from autoreactive T cells. We created transgenic mice that expressed a peptide antigen in the cortical epithelial cells of the thymus. This did not, however, result in deletion of specific T cells. Instead, antigen presentation by epithelial cells caused T cell receptor (TCR) internalization and increased gene rearrangement at the endogenous TCR alpha locus, or receptor editing. This editing mechanism in immature T cells parallels that which occurs in immature B cells, and has important implications for understanding positive and negative selection signaling in the thymus, and the limits of self-tolerance.
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pubmed:grant | |
pubmed:commentsCorrections | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1529-2908
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
1
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
336-41
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:11017106-Animals,
pubmed-meshheading:11017106-Antigen Presentation,
pubmed-meshheading:11017106-Cell Differentiation,
pubmed-meshheading:11017106-Gene Rearrangement, T-Lymphocyte,
pubmed-meshheading:11017106-Immune Tolerance,
pubmed-meshheading:11017106-Mice,
pubmed-meshheading:11017106-Mice, Inbred C57BL,
pubmed-meshheading:11017106-Receptors, Antigen, T-Cell,
pubmed-meshheading:11017106-Signal Transduction,
pubmed-meshheading:11017106-T-Lymphocytes
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pubmed:year |
2000
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pubmed:articleTitle |
Receptor editing in developing T cells.
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pubmed:affiliation |
Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN 55455, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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