Source:http://linkedlifedata.com/resource/pubmed/id/19380775
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
9
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| pubmed:dateCreated |
2009-4-21
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| pubmed:abstractText |
T cell burst size is regulated by the duration of TCR engagement and balanced control of Ag-induced activation, expansion, and apoptosis. We found that galectin-1-deficient CD8 T cells undergo greater cell division in response to TCR stimulation, with fewer dividing cells undergoing apoptosis. TCR-induced ERK signaling was sustained in activated galectin-1-deficient CD8 T cells and antagonized by recombinant galectin-1, indicating galectin-1 modulates TCR feed-forward/feedback loops involved in signal discrimination and procession. Furthermore, recombinant galectin-1 antagonized binding of agonist tetramers to the TCR on activated OT-1 T cells. Finally, galectin-1 produced by activated Ag-specific CD8 T cells negatively regulated burst size and TCR avidity in vivo. Therefore, galectin-1, inducibly expressed by activated CD8 T cells, functions as an autocrine negative regulator of peripheral CD8 T cell TCR binding, signal transduction, and burst size. Together with recent findings demonstrating that gal-1 promotes binding of agonist tetramers to the TCR of OT-1 thymocytes, these studies identify galectin-1 as a tuner of TCR binding, signaling, and functional fate determination that can differentially specify outcome, depending on the developmental and activation stage of the T cell.
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| pubmed:grant |
http://linkedlifedata.com/resource/pubmed/grant/2-T32-AI-07323,
http://linkedlifedata.com/resource/pubmed/grant/AI-28697,
http://linkedlifedata.com/resource/pubmed/grant/AI07126-30,
http://linkedlifedata.com/resource/pubmed/grant/CA-16042,
http://linkedlifedata.com/resource/pubmed/grant/R01A1056155,
http://linkedlifedata.com/resource/pubmed/grant/T32 AI07323-15
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| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
May
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| pubmed:issn |
1550-6606
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:day |
1
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| pubmed:volume |
182
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
5283-95
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| pubmed:meshHeading |
pubmed-meshheading:19380775-Animals,
pubmed-meshheading:19380775-Apoptosis,
pubmed-meshheading:19380775-Autocrine Communication,
pubmed-meshheading:19380775-CD8-Positive T-Lymphocytes,
pubmed-meshheading:19380775-Cell Differentiation,
pubmed-meshheading:19380775-Cell Division,
pubmed-meshheading:19380775-Cell Proliferation,
pubmed-meshheading:19380775-Down-Regulation,
pubmed-meshheading:19380775-Female,
pubmed-meshheading:19380775-Galectin 1,
pubmed-meshheading:19380775-Lymphocyte Activation,
pubmed-meshheading:19380775-Mice,
pubmed-meshheading:19380775-Mice, Inbred C57BL,
pubmed-meshheading:19380775-Mice, Knockout,
pubmed-meshheading:19380775-Mice, Transgenic,
pubmed-meshheading:19380775-Protein Binding,
pubmed-meshheading:19380775-Receptors, Antigen, T-Cell,
pubmed-meshheading:19380775-Signal Transduction
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| pubmed:year |
2009
|
| pubmed:articleTitle |
Galectin-1 tunes TCR binding and signal transduction to regulate CD8 burst size.
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| pubmed:affiliation |
Department of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, CA 90095-1570, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
|