| pubmed-article:1512072 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1512072 | lifeskim:mentions | umls-concept:C0021756 | lld:lifeskim |
| pubmed-article:1512072 | lifeskim:mentions | umls-concept:C0229613 | lld:lifeskim |
| pubmed-article:1512072 | lifeskim:mentions | umls-concept:C0034819 | lld:lifeskim |
| pubmed-article:1512072 | lifeskim:mentions | umls-concept:C1749467 | lld:lifeskim |
| pubmed-article:1512072 | lifeskim:mentions | umls-concept:C0021081 | lld:lifeskim |
| pubmed-article:1512072 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
| pubmed-article:1512072 | lifeskim:mentions | umls-concept:C0030685 | lld:lifeskim |
| pubmed-article:1512072 | lifeskim:mentions | umls-concept:C0443199 | lld:lifeskim |
| pubmed-article:1512072 | lifeskim:mentions | umls-concept:C0680255 | lld:lifeskim |
| pubmed-article:1512072 | lifeskim:mentions | umls-concept:C1533691 | lld:lifeskim |
| pubmed-article:1512072 | lifeskim:mentions | umls-concept:C0391871 | lld:lifeskim |
| pubmed-article:1512072 | lifeskim:mentions | umls-concept:C1283071 | lld:lifeskim |
| pubmed-article:1512072 | lifeskim:mentions | umls-concept:C1963578 | lld:lifeskim |
| pubmed-article:1512072 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:1512072 | pubmed:dateCreated | 1992-10-1 | lld:pubmed |
| pubmed-article:1512072 | pubmed:abstractText | We examined the mode of action of different immunosuppressants on the responsiveness of phytohemagglutinin (PHA)-induced lymphoblasts further stimulated by recombinant interleukin-2 (rIL-2). The stimulation of PHA blasts with rIL-2 resulted in an enhancement of tritiated thymidine ([3H]TdR) incorporation and of soluble interleukin-2 receptor (sIL-2R) release. Cyclosporin A (CsA) and prednisolone inhibited in different ways the responsiveness of PHA pre-stimulated blood mononuclear cells (PBMC) to rIL-2, as measured by [3H]TdR incorporation. The addition of CsA resulted in considerable enhancement of the release of sIL-2R, whereas the addition of prednisolone was associated with a similar enhancement only when the higher concentrations of rIL-2 were employed. EGTA, a calcium (Ca2+) chelator, and verapamil, a Ca2+ channel blocker, inhibited [3H]TdR incorporation in a concentration-dependent manner. EGTA inhibited sIL-2R release in the same manner when used alone, and reversed the CsA- and prednisolone-induced enhancement of sIL-2R release by rIL-2 induced lymphoblasts, when used in combination with CsA or prednisolone. Verapamil had a similar but less striking effect. The effects of CsA and prednisolone were also studied in PHA-induced blasts originating from purified CD4+ or CD8+ lymphocytes. Stimulation of these blasts with rIL-2 resulted in higher [3H]TdR incorporation by CD8+ blasts than by CD4+ blasts: however, no sIL-2R release was detected in supernatants of either CD4+ or of CD8+ blasts. Both CsA and prednisolone inhibited the rIL-2-induced enhancement of [3H]TdR incorporation by both T-cell subsets.(ABSTRACT TRUNCATED AT 250 WORDS) | lld:pubmed |
| pubmed-article:1512072 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1512072 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1512072 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1512072 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:1512072 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1512072 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1512072 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1512072 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1512072 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1512072 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1512072 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1512072 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1512072 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1512072 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1512072 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1512072 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:1512072 | pubmed:issn | 0192-0561 | lld:pubmed |
| pubmed-article:1512072 | pubmed:author | pubmed-author:RaskovaJJ | lld:pubmed |
| pubmed-article:1512072 | pubmed:author | pubmed-author:RaskaKKJr | lld:pubmed |
| pubmed-article:1512072 | pubmed:author | pubmed-author:DegiannisDD | lld:pubmed |
| pubmed-article:1512072 | pubmed:author | pubmed-author:HornungNN | lld:pubmed |
| pubmed-article:1512072 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1512072 | pubmed:volume | 14 | lld:pubmed |
| pubmed-article:1512072 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1512072 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1512072 | pubmed:pagination | 753-60 | lld:pubmed |
| pubmed-article:1512072 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
| pubmed-article:1512072 | pubmed:meshHeading | pubmed-meshheading:1512072-... | lld:pubmed |
| pubmed-article:1512072 | pubmed:meshHeading | pubmed-meshheading:1512072-... | lld:pubmed |
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| pubmed-article:1512072 | pubmed:meshHeading | pubmed-meshheading:1512072-... | lld:pubmed |
| pubmed-article:1512072 | pubmed:meshHeading | pubmed-meshheading:1512072-... | lld:pubmed |
| pubmed-article:1512072 | pubmed:meshHeading | pubmed-meshheading:1512072-... | lld:pubmed |
| pubmed-article:1512072 | pubmed:meshHeading | pubmed-meshheading:1512072-... | lld:pubmed |
| pubmed-article:1512072 | pubmed:meshHeading | pubmed-meshheading:1512072-... | lld:pubmed |
| pubmed-article:1512072 | pubmed:meshHeading | pubmed-meshheading:1512072-... | lld:pubmed |
| pubmed-article:1512072 | pubmed:year | 1992 | lld:pubmed |
| pubmed-article:1512072 | pubmed:articleTitle | IL-2 responsiveness of lectin-induced lymphoblasts: soluble IL-2 receptor release and differential in vitro effects of immunosuppressants. | lld:pubmed |
| pubmed-article:1512072 | pubmed:affiliation | Department of Pathology, UMDNJ-Robert Wood Johnson Medical School, Piscataway 08854. | lld:pubmed |
| pubmed-article:1512072 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1512072 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
