rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
1999-2-8
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pubmed:abstractText |
Galectin-1 is an endogenous lectin expressed by thymic and lymph node stromal cells at sites of Ag presentation and T cell death during normal development. It is known to have immunomodulatory activity in vivo and can induce apoptosis in thymocytes and activated T cells (1-3). Here we demonstrate that galectin-1 stimulation cooperates with TCR engagement to induce apoptosis, but antagonizes TCR-induced IL-2 production and proliferation in a murine T cell hybridoma and freshly isolated mouse thymocytes, respectively. Although CD4+ CD8+ double positive cells are the primary thymic subpopulation susceptible to galectin-1 treatment alone, concomitant CD3 engagement and galectin-1 stimulation broaden susceptible thymocyte subpopulations to include a subset of each CD4- CD8-, CD4+ CD8+, CD4- CD8+, and CD4+ CD8- subpopulations. Furthermore, CD3 engagement cooperates with suboptimal galectin-1 stimulation to enhance cell death in the CD4+ CD8+ subpopulation. Galectin-1 stimulation is shown to synergize with TCR engagement to dramatically and specifically enhance extracellular signal-regulated kinase-2 (ERK-2) activation, though it does not uniformly enhance TCR-induced tyrosine phosphorylation. Unlike TCR-induced IL-2 production, TCR/galectin-1-induced apoptosis is not modulated by the expression of kinase inactive or constitutively activated Lck. These data support a role for galectin-1 as a potent modulator of TCR signals and functions and indicate that individual TCR-induced signals can be independently modulated to specifically affect distinct TCR functions.
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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 |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adjuvants, Immunologic,
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD3,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD4,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD8,
http://linkedlifedata.com/resource/pubmed/chemical/Arginine,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium-Calmodulin-Dependent...,
http://linkedlifedata.com/resource/pubmed/chemical/Galectin 1,
http://linkedlifedata.com/resource/pubmed/chemical/Hemagglutinins,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Lymphocyte Specific Protein...,
http://linkedlifedata.com/resource/pubmed/chemical/Phenylalanine,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0022-1767
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
162
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
799-806
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:9916701-Adjuvants, Immunologic,
pubmed-meshheading:9916701-Animals,
pubmed-meshheading:9916701-Antibodies, Monoclonal,
pubmed-meshheading:9916701-Antigens, CD3,
pubmed-meshheading:9916701-Antigens, CD4,
pubmed-meshheading:9916701-Antigens, CD8,
pubmed-meshheading:9916701-Apoptosis,
pubmed-meshheading:9916701-Arginine,
pubmed-meshheading:9916701-Calcium-Calmodulin-Dependent Protein Kinases,
pubmed-meshheading:9916701-Cell Separation,
pubmed-meshheading:9916701-Drug Synergism,
pubmed-meshheading:9916701-Enzyme Activation,
pubmed-meshheading:9916701-Female,
pubmed-meshheading:9916701-Galectin 1,
pubmed-meshheading:9916701-Hemagglutinins,
pubmed-meshheading:9916701-Humans,
pubmed-meshheading:9916701-Hybridomas,
pubmed-meshheading:9916701-Interleukin-2,
pubmed-meshheading:9916701-Lymphocyte Activation,
pubmed-meshheading:9916701-Lymphocyte Specific Protein Tyrosine Kinase p56(lck),
pubmed-meshheading:9916701-Mice,
pubmed-meshheading:9916701-Mice, Inbred C57BL,
pubmed-meshheading:9916701-Mutagenesis, Site-Directed,
pubmed-meshheading:9916701-Phenylalanine,
pubmed-meshheading:9916701-Receptors, Antigen, T-Cell,
pubmed-meshheading:9916701-Signal Transduction,
pubmed-meshheading:9916701-T-Lymphocyte Subsets,
pubmed-meshheading:9916701-Thymus Gland
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pubmed:year |
1999
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pubmed:articleTitle |
Galectin-1 specifically modulates TCR signals to enhance TCR apoptosis but inhibit IL-2 production and proliferation.
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pubmed:affiliation |
Department of Microbiology and Immunology, University of California, Los Angeles, School of Medicine, 90095, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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