| pubmed-article:2842759 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2842759 | lifeskim:mentions | umls-concept:C0021764 | lld:lifeskim |
| pubmed-article:2842759 | lifeskim:mentions | umls-concept:C0001455 | lld:lifeskim |
| pubmed-article:2842759 | lifeskim:mentions | umls-concept:C0449258 | lld:lifeskim |
| pubmed-article:2842759 | lifeskim:mentions | umls-concept:C1552961 | lld:lifeskim |
| pubmed-article:2842759 | lifeskim:mentions | umls-concept:C1511572 | lld:lifeskim |
| pubmed-article:2842759 | lifeskim:mentions | umls-concept:C2699782 | lld:lifeskim |
| pubmed-article:2842759 | pubmed:issue | 16 | lld:pubmed |
| pubmed-article:2842759 | pubmed:dateCreated | 1988-10-5 | lld:pubmed |
| pubmed-article:2842759 | pubmed:abstractText | T lymphocytes are stimulated to proliferate in an autocrine/paracrine manner by the lymphokine interleukin 2 (IL-2). In seeking further insight into the mechanisms by which IL-2 induces progression of T cells through the G1 phase of the cell cycle, studies were performed with agents that increase cellular adenosine 3',5'-cyclic monophosphate (cAMP), a well-known inhibitor of lymphocyte growth. The addition of dibutyryl-cAMP, cholera toxin, forskolin, or 3-isobutyl-1-methylxanthine to an IL-2-dependent murine T-cell line evoked a dose-related suppression of S-phase transition without affecting cellular viability. Moreover, elevation of cAMP levels led to an accumulation of uniformly small cells, suggesting an arrest in early G1. Consistent with these findings, dibutyryl-cAMP inhibited the incorporation of both [3H]-uridine and [3H]thymidine by IL-2-stimulated, synchronized normal human T cells. Furthermore, maximal inhibition occurred during early G1, as indicated by experiments where the addition of dibutyryl-cAMP was delayed with respect to IL-2 stimulation. Quantitative flow cytometric analysis of RNA and DNA content of IL-2-stimulated cells affirmed that increased cAMP inhibits RNA accumulation and S-phase transition. In addition, exposure of IL-2-dependent, asynchronously proliferating normal human T cells to dibutyryl-cAMP resulted in uniform growth arrest in early G1, the point at which cycling T cells accumulate when they are deprived of IL-2. These results indicate that increased cAMP inhibits G1 progression stimulated by IL-2 and provide a rationale for the use of cAMP analogues as pharmacologic probes for the dissection of molecular events occurring during IL-2 signaling and T-cell G1 transit. They also suggest the possibility of therapeutic immunosuppression by a combination of agents that act at different stages of the T-cell cycle. | lld:pubmed |
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| pubmed-article:2842759 | pubmed:language | eng | lld:pubmed |
| pubmed-article:2842759 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2842759 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:2842759 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2842759 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:2842759 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:2842759 | pubmed:author | pubmed-author:SmithK AKA | lld:pubmed |
| pubmed-article:2842759 | pubmed:author | pubmed-author:DavisB HBH | lld:pubmed |
| pubmed-article:2842759 | pubmed:author | pubmed-author:JohnsonK WKW | lld:pubmed |
| pubmed-article:2842759 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2842759 | pubmed:volume | 85 | lld:pubmed |
| pubmed-article:2842759 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2842759 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2842759 | pubmed:pagination | 6072-6 | lld:pubmed |
| pubmed-article:2842759 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:2842759 | pubmed:year | 1988 | lld:pubmed |
| pubmed-article:2842759 | pubmed:articleTitle | cAMP antagonizes interleukin 2-promoted T-cell cycle progression at a discrete point in early G1. | lld:pubmed |
| pubmed-article:2842759 | pubmed:affiliation | Department of Medicine, Dartmouth Medical School, Hanover, NH 03756. | lld:pubmed |
| pubmed-article:2842759 | pubmed:publicationType | Journal Article | lld:pubmed |
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