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rdf:type |
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lifeskim:mentions |
umls-concept:C0011155,
umls-concept:C0026809,
umls-concept:C0034790,
umls-concept:C0039194,
umls-concept:C0205263,
umls-concept:C0330390,
umls-concept:C1421567,
umls-concept:C1424685,
umls-concept:C1527940,
umls-concept:C1705831,
umls-concept:C1710082,
umls-concept:C2003941
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pubmed:issue |
1
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pubmed:dateCreated |
2000-9-15
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pubmed:abstractText |
The mechanism of development of a unique subset of T cells, thymic NK1.1(+) alpha beta T cells, has been poorly understood. We found that the development of thymic NK1.1(+) alpha beta T cells was defective in mice deficient in ZAP-70. Instead, an accumulation of NK1.1(+) TCR beta(-) NK-like population was detected in the thymus and spleen of the ZAP-70 deficient (ZAP -/-) mouse. In the present report, we examined whether biochemical treatments that replace TCR-mediated positive selection signals could restore the generation of thymic NK1.1(+) alpha beta T cells in ZAP -/- mice using the thymus organ culture. We found that a higher concentration of phorbol ester (PMA) than that required for CD4(+) T cell generation and ionomycin induced the generation of NK1.1(+) alpha beta T cells. Phenotypic analysis of the induced NK1.1(+) alpha beta T cell population suggested that these cells expressed CD8 but not CD4 molecules, which is a different characteristic from ordinary thymic NK1.1(+) alpha beta T cells. These results suggest that differential signaling is required for the generation of mainstream T cells and thymic NK1.1(+) alpha beta T cells.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Ly,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Surface,
http://linkedlifedata.com/resource/pubmed/chemical/Ionomycin,
http://linkedlifedata.com/resource/pubmed/chemical/Ionophores,
http://linkedlifedata.com/resource/pubmed/chemical/Klrb1c protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Lectins, C-Type,
http://linkedlifedata.com/resource/pubmed/chemical/NK Cell Lectin-Like Receptor...,
http://linkedlifedata.com/resource/pubmed/chemical/Phorbol Esters,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Tyrosine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell...,
http://linkedlifedata.com/resource/pubmed/chemical/ZAP-70 Protein-Tyrosine Kinase,
http://linkedlifedata.com/resource/pubmed/chemical/Zap70 protein, mouse
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0165-2478
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
3
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pubmed:volume |
73
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
65-9
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:10963813-Animals,
pubmed-meshheading:10963813-Animals, Newborn,
pubmed-meshheading:10963813-Antigens,
pubmed-meshheading:10963813-Antigens, Ly,
pubmed-meshheading:10963813-Antigens, Surface,
pubmed-meshheading:10963813-CD8-Positive T-Lymphocytes,
pubmed-meshheading:10963813-Cell Differentiation,
pubmed-meshheading:10963813-Cell Division,
pubmed-meshheading:10963813-Ionomycin,
pubmed-meshheading:10963813-Ionophores,
pubmed-meshheading:10963813-Lectins, C-Type,
pubmed-meshheading:10963813-Lymphocyte Subsets,
pubmed-meshheading:10963813-Mice,
pubmed-meshheading:10963813-Mice, Knockout,
pubmed-meshheading:10963813-NK Cell Lectin-Like Receptor Subfamily B,
pubmed-meshheading:10963813-Organ Culture Techniques,
pubmed-meshheading:10963813-Phorbol Esters,
pubmed-meshheading:10963813-Protein-Tyrosine Kinases,
pubmed-meshheading:10963813-Proteins,
pubmed-meshheading:10963813-Receptors, Antigen, T-Cell, alpha-beta,
pubmed-meshheading:10963813-T-Lymphocytes,
pubmed-meshheading:10963813-Thymus Gland,
pubmed-meshheading:10963813-ZAP-70 Protein-Tyrosine Kinase
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pubmed:year |
2000
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pubmed:articleTitle |
Induction of NK1.1(+) alpha beta TCR(+) T cells by bypassing TCR signals in ZAP-70 deficient mice.
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pubmed:affiliation |
Division of Immunobiology, Section of Pathophysiology, Institute for Genetic Medicine, Hokkaido University, Kita-15 Nishi-7, Kita-Ku, Sapporo 060-0815, Japan.
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pubmed:publicationType |
Journal Article
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