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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
8 Pt 1
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pubmed:dateCreated |
1993-5-12
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pubmed:abstractText |
Transforming growth factors-beta (TGF-beta) modulate immune responses by inhibiting the proliferation of normal T lymphocytes. To examine the mechanism(s) of this inhibition, we studied the effect of TGF-beta 1 on selected events associated with the initiation and progression of the T lymphocyte cell cycle. Human peripheral blood T cells were stimulated with anti-CD3 mAb, PHA, PMA, or ionomycin, alone or in combination. TGF-beta 1 (0.5 to 10 ng/ml) partially inhibited the tyrosine phosphorylation of a 100-kDa protein, but not the calcium influx when cells were stimulated via TCR. Nuclear transcription of early activation genes (c-fos, c-jun, and c-myc) as determined by nuclear run-off assays, and steady state mRNA levels and/or protein products of intermediate activation genes (IL-2, IL-2R alpha, IL-2R beta, and transferrin receptor) were not affected by TGF-beta 1. Total cellular RNA synthesis and cell size after T cell stimulation were also not affected by TGF-beta 1. However, TGF-beta 1 inhibited the IL-2-dependent proliferation of Con A lymphoblasts by -50%. This inhibition was associated with the down-regulation of IL-2-mediated tyrosine phosphorylation of proteins of 120, 100, 85, 75, and 50 kDa. TGF-beta 1 also inhibited the IL-2-dependent phosphorylation of the retinoblastoma susceptibility gene product, which plays an important role in cell cycle progression. These results suggest that TGF-beta 1 inhibits T cell proliferation by down-regulating predominantly IL-2-mediated proliferative signals.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD3,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Retinoblastoma Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta,
http://linkedlifedata.com/resource/pubmed/chemical/Tyrosine
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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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 |
150
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3109-18
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pubmed:dateRevised |
2004-11-17
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pubmed:meshHeading |
pubmed-meshheading:8468460-Adult,
pubmed-meshheading:8468460-Antibodies, Monoclonal,
pubmed-meshheading:8468460-Antigens, CD3,
pubmed-meshheading:8468460-Cells, Cultured,
pubmed-meshheading:8468460-Gene Expression,
pubmed-meshheading:8468460-Humans,
pubmed-meshheading:8468460-Interleukin-2,
pubmed-meshheading:8468460-Lymphocyte Activation,
pubmed-meshheading:8468460-Phosphorylation,
pubmed-meshheading:8468460-Receptors, Interleukin-2,
pubmed-meshheading:8468460-Retinoblastoma Protein,
pubmed-meshheading:8468460-T-Lymphocytes,
pubmed-meshheading:8468460-Transcription, Genetic,
pubmed-meshheading:8468460-Transforming Growth Factor beta,
pubmed-meshheading:8468460-Tyrosine
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pubmed:year |
1993
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pubmed:articleTitle |
Effect of transforming growth factor-beta on early and late activation events in human T cells.
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pubmed:affiliation |
Kidney Disease Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892.
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pubmed:publicationType |
Journal Article
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