Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
|
pubmed:dateCreated |
1998-6-30
|
pubmed:abstractText |
Organ-specific autoimmune disease can be caused by alphabeta T cells that have escaped self-tolerance induction. Here we show that one of the causes of escape from self-tolerance is the coexpression of two different T cell receptors by the same cell, which can occur in up to 30% of all T cells in normal mice and can lead to low-level surface expression of an autospecific TCR. We found that double receptor-expressing T cells can escape tolerance even to ubiquitously expressed antigens but can nevertheless induce autoimmune diabetes when the relevant protein is expressed in pancreatic tissue. Such diabetogenic T cells are absent, however, among T cells expressing the autospecific TCR as the sole receptor.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:month |
May
|
pubmed:issn |
1074-7613
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
8
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
563-70
|
pubmed:dateRevised |
2011-11-17
|
pubmed:meshHeading |
pubmed-meshheading:9620677-Alleles,
pubmed-meshheading:9620677-Animals,
pubmed-meshheading:9620677-Autoimmunity,
pubmed-meshheading:9620677-CD4-Positive T-Lymphocytes,
pubmed-meshheading:9620677-Diabetes Mellitus, Type 1,
pubmed-meshheading:9620677-Hemagglutinin Glycoproteins, Influenza Virus,
pubmed-meshheading:9620677-Insulin,
pubmed-meshheading:9620677-Mice,
pubmed-meshheading:9620677-Mice, Inbred BALB C,
pubmed-meshheading:9620677-Mice, Transgenic,
pubmed-meshheading:9620677-Pancreas,
pubmed-meshheading:9620677-Promoter Regions, Genetic,
pubmed-meshheading:9620677-Rats,
pubmed-meshheading:9620677-Receptors, Antigen, T-Cell, alpha-beta,
pubmed-meshheading:9620677-Self Tolerance
|
pubmed:year |
1998
|
pubmed:articleTitle |
Allelic inclusion of T cell receptor alpha genes poses an autoimmune hazard due to low-level expression of autospecific receptors.
|
pubmed:affiliation |
Institut Necker, INSERM 373, Paris, France.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|