pubmed-article:2174560 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:2174560 | lifeskim:mentions | umls-concept:C0021756 | lld:lifeskim |
pubmed-article:2174560 | lifeskim:mentions | umls-concept:C0021758 | lld:lifeskim |
pubmed-article:2174560 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
pubmed-article:2174560 | lifeskim:mentions | umls-concept:C0001455 | lld:lifeskim |
pubmed-article:2174560 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:2174560 | pubmed:issue | 23 | lld:pubmed |
pubmed-article:2174560 | pubmed:dateCreated | 1991-1-16 | lld:pubmed |
pubmed-article:2174560 | pubmed:abstractText | In this report, we explore the nature of the inductive stimuli leading to expression of the divergently regulated lymphokines interleukin 2 (IL-2) and interleukin 4 (IL-4). Elevation of cAMP levels blocks IL-2 induction while sparing IL-4 induction. These effects are gene-specific, not cell-specific, and can be observed in the same cells. Transient transfection experiments using murine IL-2 regulatory sequences to drive expression of a reporter gene show at least part of the inhibition to act at the transcriptional level. The possible biological significance of these results is indicated by the observation that representative type 2 helper T-cell lines maintain significantly higher levels of cAMP per cell than a type 1 helper T-cell line. Fresh splenic CD4+ T cells, which preferentially make IL-2, have particularly low levels of cAMP per cell and a low capacity to elevate cAMP in response to forskolin. However, their response to forskolin increases significantly after several days of stimulation. These results suggest a potential link between differential cAMP regulation and the divergence of memory T cells into effector subsets. | lld:pubmed |
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pubmed-article:2174560 | pubmed:language | eng | lld:pubmed |
pubmed-article:2174560 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2174560 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:2174560 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:2174560 | pubmed:month | Dec | lld:pubmed |
pubmed-article:2174560 | pubmed:issn | 0027-8424 | lld:pubmed |
pubmed-article:2174560 | pubmed:author | pubmed-author:NovakT JTJ | lld:pubmed |
pubmed-article:2174560 | pubmed:author | pubmed-author:RothenbergE... | lld:pubmed |
pubmed-article:2174560 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:2174560 | pubmed:volume | 87 | lld:pubmed |
pubmed-article:2174560 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:2174560 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:2174560 | pubmed:pagination | 9353-7 | lld:pubmed |
pubmed-article:2174560 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:2174560 | pubmed:year | 1990 | lld:pubmed |
pubmed-article:2174560 | pubmed:articleTitle | cAMP inhibits induction of interleukin 2 but not of interleukin 4 in T cells. | lld:pubmed |
pubmed-article:2174560 | pubmed:affiliation | Division of Biology, California Institute of Technology, Pasadena 91125. | lld:pubmed |
pubmed-article:2174560 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:2174560 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |