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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5
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pubmed:dateCreated |
1991-12-13
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pubmed:abstractText |
Glucocorticoids (GC) modulate immune function in a number of ways, including suppression of T cell proliferation and other IL-2-mediated T cell functions. These inhibitory effects are similar to those induced by transforming growth factor-beta 1 (TGF-beta 1), a cytokine with potent T cell inhibiting activities. We examined the hypothesis that GC effects may be at least partially achieved through modulation of the expression of the TGF-beta 1 gene in activated T cells. Normal T cells were cultured with or without purified phytohemagglutinin (PHA-p) and 4 beta-phorbol 12-myristate 13-acetate (PMA) in the presence or absence of the synthetic GC, dexamethasone (100-200 micrograms/ml). The production of latent and active forms of TGF beta by these cells were analyzed by immunoblotting and bioassays. The steady-state levels of TGF-beta 1 mRNA were analyzed in total RNA from these cells by Northern hybridizations using a human TGF-beta 1 cDNA. The results showed that dexamethasone caused an increase in TGF beta production and a dose-dependent two to fourfold increase in TGF-beta 1 mRNA in activated as well as in unstimulated T cells, 1 h after exposure of the cultures to the steroid. The increase in TGF-beta 1 mRNA levels by dexamethasone was further potentiated two to threefold by cycloheximide, suggesting that the steroid effect may be due to inhibition of the synthesis of proteins that decrease TGF-beta 1 gene transcription or the stability of its transcripts. Finally, in vitro nuclear transcription studies indicated the dexamethasone effects on TGF-beta 1 gene expression to be largely transcriptional.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/1939646-1979585,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1939646-2175324,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/1939646-96133
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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 |
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0021-9738
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
88
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1574-80
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:1939646-Cells, Cultured,
pubmed-meshheading:1939646-Cycloheximide,
pubmed-meshheading:1939646-Dexamethasone,
pubmed-meshheading:1939646-Gene Expression Regulation,
pubmed-meshheading:1939646-Humans,
pubmed-meshheading:1939646-Lymphocyte Activation,
pubmed-meshheading:1939646-T-Lymphocytes,
pubmed-meshheading:1939646-Transcription, Genetic,
pubmed-meshheading:1939646-Transforming Growth Factor beta
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pubmed:year |
1991
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pubmed:articleTitle |
Regulation of transforming growth factor-beta 1 gene expression by glucocorticoids in normal human T lymphocytes.
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pubmed:affiliation |
Cardeza Foundation for Hematologic Research, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania 19107.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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