| pubmed-article:1702375 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1702375 | lifeskim:mentions | umls-concept:C0005841 | lld:lifeskim |
| pubmed-article:1702375 | lifeskim:mentions | umls-concept:C0022144 | lld:lifeskim |
| pubmed-article:1702375 | lifeskim:mentions | umls-concept:C0024262 | lld:lifeskim |
| pubmed-article:1702375 | lifeskim:mentions | umls-concept:C0010592 | lld:lifeskim |
| pubmed-article:1702375 | lifeskim:mentions | umls-concept:C0033268 | lld:lifeskim |
| pubmed-article:1702375 | lifeskim:mentions | umls-concept:C0729218 | lld:lifeskim |
| pubmed-article:1702375 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:1702375 | pubmed:dateCreated | 1991-2-14 | lld:pubmed |
| pubmed-article:1702375 | pubmed:abstractText | The effect of administration of cyclosporin A (CyA) or the novel macrolide FK506 was investigated in AO rats given DA blood transfusions. CyA (10 mg/kg, orally) or FK506 (1 mg/kg, intramuscularly) administered for 14 days from the time of transfusion effectively inhibited primary anti-MHC class I alloantibody production. This profound inhibitory effect persisted throughout the 2-month investigation period, with little increase in 'secondary' alloantibody production following a challenge injection 28 days after drug withdrawal. Flow cytometric analysis revealed no significant differences in the absolute numbers of W3/25+ (CD4+), OX-8+ (CD8+) or OX-12+ (B lymphocytes), in either the spleen or peripheral blood of transfused compared with normal, untreated animals. However, a small but significant increase in the numbers of splenocytes expressing the activation marker OX-40 (activated CD4+ cells) was observed in transfused animals. Either CyA or FK506 significantly reduced the number of cells expressing OX-39 (interleukin-2 receptors) and OX-40. Treatment of transfused animals with CyA, but not FK506 for 14 days resulted in minor, transient reduction in peripheral blood OX-19+ and W3/25+ cells, while 'sparing' the OX-8+ cells; these changes were not observed in spleens. In contrast, the absolute spleen cell numbers of OX-19+, W3/25+ and OX-8+ cells were significantly reduced in transfused animals given 14 days of FK506 treatment, while the corresponding blood cells were unaffected. Induction of splenic lymphoproliferative responses by the T cell mitogen concanavalin A remained normal in animals receiving transfusion alone or with CyA. In contrast, profound inhibition of mitogenic responses was observed in FK506-treated animals and this inhibitory effect declined gradually following drug withdrawal. No non-specific suppressor cell activity was detected in the spleens of rats given transfusion alone or in CyA or FK506-treated transfused animals. | lld:pubmed |
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| pubmed-article:1702375 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:1702375 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:1702375 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1702375 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:1702375 | pubmed:issn | 0009-9104 | lld:pubmed |
| pubmed-article:1702375 | pubmed:author | pubmed-author:ThomsonA WAW | lld:pubmed |
| pubmed-article:1702375 | pubmed:author | pubmed-author:WooJJ | lld:pubmed |
| pubmed-article:1702375 | pubmed:author | pubmed-author:MacleodA MAM | lld:pubmed |
| pubmed-article:1702375 | pubmed:author | pubmed-author:PropperD JDJ | lld:pubmed |
| pubmed-article:1702375 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1702375 | pubmed:volume | 82 | lld:pubmed |
| pubmed-article:1702375 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1702375 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1702375 | pubmed:pagination | 462-8 | lld:pubmed |
| pubmed-article:1702375 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:1702375 | pubmed:year | 1990 | lld:pubmed |
| pubmed-article:1702375 | pubmed:articleTitle | Influence of FK506 and cyclosporin A on alloantibody production and lymphocyte activation following blood transfusion. | lld:pubmed |
| pubmed-article:1702375 | pubmed:affiliation | Department of Pathology, University of Aberdeen, Scotland. | lld:pubmed |
| pubmed-article:1702375 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1702375 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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