pubmed-article:1939646 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:1939646 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
pubmed-article:1939646 | lifeskim:mentions | umls-concept:C1704256 | lld:lifeskim |
pubmed-article:1939646 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
pubmed-article:1939646 | lifeskim:mentions | umls-concept:C0017710 | lld:lifeskim |
pubmed-article:1939646 | lifeskim:mentions | umls-concept:C0205307 | lld:lifeskim |
pubmed-article:1939646 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
pubmed-article:1939646 | lifeskim:mentions | umls-concept:C1515406 | lld:lifeskim |
pubmed-article:1939646 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
pubmed-article:1939646 | pubmed:issue | 5 | lld:pubmed |
pubmed-article:1939646 | pubmed:dateCreated | 1991-12-13 | lld:pubmed |
pubmed-article:1939646 | 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. | lld:pubmed |
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pubmed-article:1939646 | pubmed:language | eng | lld:pubmed |
pubmed-article:1939646 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1939646 | pubmed:citationSubset | AIM | lld:pubmed |
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pubmed-article:1939646 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:1939646 | pubmed:month | Nov | lld:pubmed |
pubmed-article:1939646 | pubmed:issn | 0021-9738 | lld:pubmed |
pubmed-article:1939646 | pubmed:author | pubmed-author:JimenezS ASA | lld:pubmed |
pubmed-article:1939646 | pubmed:author | pubmed-author:DiazAA | lld:pubmed |
pubmed-article:1939646 | pubmed:author | pubmed-author:AyanlarBatuma... | lld:pubmed |
pubmed-article:1939646 | pubmed:author | pubmed-author:FerreroA PAP | lld:pubmed |
pubmed-article:1939646 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:1939646 | pubmed:volume | 88 | lld:pubmed |
pubmed-article:1939646 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:1939646 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:1939646 | pubmed:pagination | 1574-80 | lld:pubmed |
pubmed-article:1939646 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
pubmed-article:1939646 | pubmed:meshHeading | pubmed-meshheading:1939646-... | lld:pubmed |
pubmed-article:1939646 | pubmed:meshHeading | pubmed-meshheading:1939646-... | lld:pubmed |
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pubmed-article:1939646 | pubmed:meshHeading | pubmed-meshheading:1939646-... | lld:pubmed |
pubmed-article:1939646 | pubmed:year | 1991 | lld:pubmed |
pubmed-article:1939646 | pubmed:articleTitle | Regulation of transforming growth factor-beta 1 gene expression by glucocorticoids in normal human T lymphocytes. | lld:pubmed |
pubmed-article:1939646 | pubmed:affiliation | Cardeza Foundation for Hematologic Research, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania 19107. | lld:pubmed |
pubmed-article:1939646 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:1939646 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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