Linked Life Data

11279170

Source:http://linkedlifedata.com/resource/pubmed/id/11279170

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
20
pubmed:dateCreated
2001-5-23
pubmed:abstractText
Human thymic CD1a-CD4+ T cells in the final stage of thymic maturation are susceptible to anergy induced by a superantigen, toxic shock syndrome toxin-1 (TSST-1). Thymic CD4+ T-cell blasts, established by stimulating human thymic CD1a-CD4+ T cells with TSST-1 in vitro, produce a low level of interleukin-2 after restimulation with TSST-1, whereas TSST-1-induced adult peripheral blood (APB) CD4+ T-cell blasts produce high levels of interleukin-2. The extent of tyrosine phosphorylation of the T-cell receptor zeta chain induced after restimulation with TSST-1 was 2-4-fold higher in APB CD4+ T-cell blasts than in thymic CD4+ T-cell blasts. The tyrosine kinase activity of Lck was low in both thymic and APB CD4+ T-cell blasts before restimulation with TSST-1. After restimulation, the Lck kinase activity increased in APB CD4+ T-cell blasts but not in thymic CD4+ T-cell blasts. Surprisingly, Lck was highly tyrosine-phosphorylated in both thymic and APB CD4+ T-cell blasts before restimulation with TSST-1. After restimulation, it was markedly dephosphorylated in APB CD4+ T-cell blasts but not in thymic CD4+ T-cell blasts. Lck from APB CD4+ T-cell blasts bound the peptide containing the phosphotyrosine at the negative regulatory site of Lck-505 indicating that the site of dephosphorylation in TSST-1-activated T-cell blasts is Tyr-505. Confocal microscopy demonstrated that colocalization of Lck and CD45 was induced after restimulation with TSST-1 in APB CD4+ T-cell blasts but not in thymic CD4+ T-cell blasts. Further, remarkable accumulation of Lck in the membrane raft was observed in restimulated APB CD4+ T-cell blasts but not in thymic CD4+ T-cell blasts. These data indicate that interaction between Lck and CD45 is suppressed physically in thymic CD4+ T-cell blasts and plays a critical role in sustaining an anergic state.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
18
pubmed:volume
276
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
17455-60
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:11279170-Adult, pubmed-meshheading:11279170-Animals, pubmed-meshheading:11279170-Antigen-Presenting Cells, pubmed-meshheading:11279170-Bacterial Toxins, pubmed-meshheading:11279170-CD4-Positive T-Lymphocytes, pubmed-meshheading:11279170-Cells, Cultured, pubmed-meshheading:11279170-Clonal Anergy, pubmed-meshheading:11279170-Enterotoxins, pubmed-meshheading:11279170-Humans, pubmed-meshheading:11279170-Interleukin-2, pubmed-meshheading:11279170-L Cells (Cell Line), pubmed-meshheading:11279170-Lymphocyte Activation, pubmed-meshheading:11279170-Lymphocyte Specific Protein Tyrosine Kinase p56(lck), pubmed-meshheading:11279170-Mice, pubmed-meshheading:11279170-Models, Immunological, pubmed-meshheading:11279170-Receptors, Antigen, T-Cell, pubmed-meshheading:11279170-Rosette Formation, pubmed-meshheading:11279170-Sheep, pubmed-meshheading:11279170-Superantigens, pubmed-meshheading:11279170-T-Lymphocytes, pubmed-meshheading:11279170-Thymus Gland
pubmed:year
2001
pubmed:articleTitle
Functional uncoupling of T-cell receptor engagement and Lck activation in anergic human thymic CD4+ T cells.
pubmed:affiliation
Department of Microbiology and Immunology, The Heart Institute of Japan, Tokyo Women's Medical University, Tokyo 162-8666, Japan. wakae@research.twmu.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't