| pubmed-article:2246324 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2246324 | lifeskim:mentions | umls-concept:C0021756 | lld:lifeskim |
| pubmed-article:2246324 | lifeskim:mentions | umls-concept:C0022688 | lld:lifeskim |
| pubmed-article:2246324 | lifeskim:mentions | umls-concept:C0596402 | lld:lifeskim |
| pubmed-article:2246324 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
| pubmed-article:2246324 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:2246324 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:2246324 | pubmed:dateCreated | 1991-1-8 | lld:pubmed |
| pubmed-article:2246324 | pubmed:abstractText | The activation of human natural killer (NK) cell cytotoxicity by interleukin 2 (IL-2) is well established, although the biochemical mechanisms of this stimulation have not yet been fully delineated. Earlier, we reported that treatment of NK cells with an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase such as compactin or lovastatin significantly abrogates the in vitro killing of a susceptible human erythroleukemic cell line and that this inhibition can be completely reversed by 2 hr of exposure to mevalonate (J. Cell. Physiology 139:550-557, 1989). We report here that 24 hr of treatment with IL-2 also reverses lovastatin inhibition of NK cell function. In addition to natural cytotoxicity, IL-2 also restores chemotactic and antibody dependent cellular cytotoxicity functions to lovastatin-treated cells. IL-2 does not stimulate proliferation of these cells during this time period, nor does it affect the phenotypic composition of the NK cell preparations. Although IL-2 was able to reverse the lovastatin-mediated inhibition of every cell function we examined, it had no effect on the inhibition of cholesterol biosynthesis as measured by [3H]acetate incorporation into non-saponifiable lipids, nor did it stimulate HMG CoA reductase activity. These findings support the hypothesis that there is a non-sterol isoprenoid product which is required for NK cell cytotoxicity and chemotaxis. In addition, the data suggest that IL-2 stimulation of NK cells proceeds by an isoprenoid-independent pathway. | lld:pubmed |
| pubmed-article:2246324 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2246324 | pubmed:language | eng | lld:pubmed |
| pubmed-article:2246324 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2246324 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:2246324 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:2246324 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2246324 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:2246324 | pubmed:issn | 0021-9541 | lld:pubmed |
| pubmed-article:2246324 | pubmed:author | pubmed-author:BankhurstA... | lld:pubmed |
| pubmed-article:2246324 | pubmed:author | pubmed-author:CuttsJ LJL | lld:pubmed |
| pubmed-article:2246324 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2246324 | pubmed:volume | 145 | lld:pubmed |
| pubmed-article:2246324 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2246324 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2246324 | pubmed:pagination | 244-52 | lld:pubmed |
| pubmed-article:2246324 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:2246324 | pubmed:meshHeading | pubmed-meshheading:2246324-... | lld:pubmed |
| pubmed-article:2246324 | pubmed:year | 1990 | lld:pubmed |
| pubmed-article:2246324 | pubmed:articleTitle | Reversal of lovastatin-mediated inhibition of natural killer cell cytotoxicity by interleukin 2. | lld:pubmed |
| pubmed-article:2246324 | pubmed:affiliation | Department of Medicine, School of Medicine, University of New Mexico, Albuquerque 87131. | lld:pubmed |
| pubmed-article:2246324 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:2246324 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:2246324 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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