Source:http://linkedlifedata.com/resource/pubmed/id/10580999
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2000-1-5
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pubmed:abstractText |
Stimulation of T cells by the T-cell receptor (TCR)/CD3 complex results in interleukin-2 (IL-2) synthesis and surface expression of the IL-2 receptor (IL-2R), which in turn drive T-cell proliferation. However, the significance of the requirement of IL-2 in driving T-cell proliferation, when TCR stimulation itself delivers potential mitogenic signals, is unclear. We show that blocking of IL-2 synthesis by Cyclosporin A (CsA) suppressed both the Concanavalin A (Con A)- and phorbol myristate acetate (PMA)/ionomycin-induced proliferation of T cells. The latter is also inhibited by anti-IL-2R. Kinetic studies showed that T-cell proliferation begins to become resistant to CsA inhibition by about 12 h and became largely resistant by 18 h of stimulation. PMA, the protein kinase C activator, enhanced Con A-induced T-cell proliferation if added only within first 12 h of stimulation, and not after that. Given the fact that, in the present study, TCR is downregulated within 2 h of Con A stimulation and T cells entered the S phase of cell cycle by about 18 h of stimulation, the above results suggest that TCR stimulation provides the initial trigger to the resting T cells, which allows the cells to traverse the first two third portions of G1 phase of cell cycle and become proliferation competent. IL-2 action begins afterward, delivering the actual proliferation signal(s), allowing the cells to traverse the rest of G1 phase and enter the S phase of the cell cycle.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Concanavalin A,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Ligands,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0730-2312
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pubmed:author | |
pubmed:copyrightInfo |
Copyright 1999 Wiley-Liss, Inc.
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pubmed:issnType |
Print
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pubmed:volume |
76
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
37-43
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:10580999-Animals,
pubmed-meshheading:10580999-Cell Division,
pubmed-meshheading:10580999-Concanavalin A,
pubmed-meshheading:10580999-G1 Phase,
pubmed-meshheading:10580999-Interleukin-2,
pubmed-meshheading:10580999-Ligands,
pubmed-meshheading:10580999-Mice,
pubmed-meshheading:10580999-Mice, Inbred BALB C,
pubmed-meshheading:10580999-Protein Kinase C,
pubmed-meshheading:10580999-Receptors, Antigen, T-Cell,
pubmed-meshheading:10580999-S Phase,
pubmed-meshheading:10580999-Signal Transduction,
pubmed-meshheading:10580999-T-Lymphocytes
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pubmed:year |
1999
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pubmed:articleTitle |
Relative roles of T-cell receptor ligands and interleukin-2 in driving T-cell proliferation.
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pubmed:affiliation |
Molecular Biology Unit, Institute of Medical Sciences, Banaras Hindu University, Varanasi 221005, India.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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