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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2006-7-24
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pubmed:abstractText |
The paradigm to explain antigen-dependent T cell receptor (TCR) signaling is based on the activation of the CD4 or CD8 coreceptor-associated kinase Lck. It is widely assumed that this paradigm is also applicable to signaling by bacterial superantigens. However, these bacterial toxins can activate human T cells lacking Lck, suggesting the existence of an additional pathway of TCR signaling. Here we showed that this alternative pathway operates in the absence of Lck-dependent tyrosine-phosphorylation events and was initiated by the TCR-dependent activation of raft-enriched heterotrimeric Galpha11 proteins. This event, in turn, activated a phospholipase C-beta and protein kinase C-mediated cascade that turned on the mitogen-activated protein kinases ERK-1 and ERK-2, triggered Ca(2+) influx, and translocated the transcription factors NF-AT and NF-kappaB to the nucleus, ultimately inducing the production of interleukin-2 in Lck-deficient T cells. The triggering of this alternative pathway by superantigens suggests that these toxins use a G protein-coupled receptor as a coreceptor on T cells.
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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 |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Bacterial,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD4,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Enterotoxins,
http://linkedlifedata.com/resource/pubmed/chemical/Extracellular Signal-Regulated MAP...,
http://linkedlifedata.com/resource/pubmed/chemical/GTP-Binding Protein alpha...,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Isoenzymes,
http://linkedlifedata.com/resource/pubmed/chemical/Lymphocyte Specific Protein...,
http://linkedlifedata.com/resource/pubmed/chemical/Phospholipase C beta,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphoserine,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell,
http://linkedlifedata.com/resource/pubmed/chemical/Superantigens,
http://linkedlifedata.com/resource/pubmed/chemical/Type C Phospholipases,
http://linkedlifedata.com/resource/pubmed/chemical/enterotoxin E, Staphylococcal
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
1074-7613
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
25
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
67-78
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:16860758-Antigens, Bacterial,
pubmed-meshheading:16860758-Antigens, CD4,
pubmed-meshheading:16860758-Calcium,
pubmed-meshheading:16860758-Cells, Cultured,
pubmed-meshheading:16860758-Enterotoxins,
pubmed-meshheading:16860758-Enzyme Activation,
pubmed-meshheading:16860758-Extracellular Signal-Regulated MAP Kinases,
pubmed-meshheading:16860758-GTP-Binding Protein alpha Subunits, Gq-G11,
pubmed-meshheading:16860758-Humans,
pubmed-meshheading:16860758-Interleukin-2,
pubmed-meshheading:16860758-Isoenzymes,
pubmed-meshheading:16860758-Lymphocyte Activation,
pubmed-meshheading:16860758-Lymphocyte Specific Protein Tyrosine Kinase p56(lck),
pubmed-meshheading:16860758-Phospholipase C beta,
pubmed-meshheading:16860758-Phosphoserine,
pubmed-meshheading:16860758-Protein Kinase C,
pubmed-meshheading:16860758-Receptors, Antigen, T-Cell,
pubmed-meshheading:16860758-Signal Transduction,
pubmed-meshheading:16860758-Superantigens,
pubmed-meshheading:16860758-Type C Phospholipases
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pubmed:year |
2006
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pubmed:articleTitle |
Bacterial superantigens bypass Lck-dependent T cell receptor signaling by activating a Galpha11-dependent, PLC-beta-mediated pathway.
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pubmed:affiliation |
The FOCIS Centre for Clinical Immunology and Immunotherapeutics, London, Ontario N6A 5K8, Canada.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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