Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
11
|
| pubmed:dateCreated |
1994-12-29
|
| pubmed:abstractText |
Posttransplant patients undergoing prolonged cyclosporine A (CsA) immunosuppressive therapy have been reported to have increased incidence of Epstein-Barr virus (EBV)-associated lymphoproliferative disorders. We undertook experiments to analyze the possible actions of CsA during EBV-infection of human peripheral blood mononuclear cells (PBMC). EBV-infected B cells cultured with CsA demonstrated increased EBV B-cell outgrowth as compared with those cultured without CsA. PBMC, after infection with EBV and CsA treatment, demonstrated increased interleukin-6 (IL-6) activity in the culture supernatant. The induction of IL-6 appears to differ within the various lymphocyte populations. In monocytes, IL-6 expression appears preferentially induced by EBV and is initiated by the binding of the two major virion glycoproteins, gp350 and gp220. Expression of IL-6 in T cells appears to be due mainly to CsA. B cells also express IL-6 after EBV exposure, but not after CsA treatment. EBV-immortalized B-cell lines cultured with CsA exhibited both an increased number of cells expressing viral lytic-cycle antigens and increased amounts of lytic-cycle proteins. IL-6, which is induced by CsA in PBMC, was also capable of inducing the lytic viral cycle in several EBV-immortalized cells. CsA, in promoting both increased numbers of lytic EBV B cells and an EBV paracrine factor, IL-6, within the microenvironment of EBV B cell:T cell and EBV B cell:monocyte interactions, may result in increased EBV B-cell immortalization and ultimately lead to the promotion of B-cell lymphomas in immunosuppressed patients.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Viral,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclosporine,
http://linkedlifedata.com/resource/pubmed/chemical/EBV-associated membrane antigen...,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/Ionomycin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Complement 3d,
http://linkedlifedata.com/resource/pubmed/chemical/Tetradecanoylphorbol Acetate,
http://linkedlifedata.com/resource/pubmed/chemical/Viral Matrix Proteins
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Dec
|
| pubmed:issn |
0006-4971
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
1
|
| pubmed:volume |
84
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
3956-64
|
| pubmed:dateRevised |
2006-11-15
|
| pubmed:meshHeading |
pubmed-meshheading:7949151-Antigens, Viral,
pubmed-meshheading:7949151-B-Lymphocytes,
pubmed-meshheading:7949151-Cell Transformation, Viral,
pubmed-meshheading:7949151-Cells, Cultured,
pubmed-meshheading:7949151-Cyclosporine,
pubmed-meshheading:7949151-Gene Expression Regulation, Viral,
pubmed-meshheading:7949151-Herpesvirus 4, Human,
pubmed-meshheading:7949151-Humans,
pubmed-meshheading:7949151-Immunocompromised Host,
pubmed-meshheading:7949151-Interleukin-6,
pubmed-meshheading:7949151-Ionomycin,
pubmed-meshheading:7949151-Lymphoma, B-Cell,
pubmed-meshheading:7949151-Lymphoproliferative Disorders,
pubmed-meshheading:7949151-Monocytes,
pubmed-meshheading:7949151-Polymerase Chain Reaction,
pubmed-meshheading:7949151-Receptors, Complement 3d,
pubmed-meshheading:7949151-Stimulation, Chemical,
pubmed-meshheading:7949151-Tetradecanoylphorbol Acetate,
pubmed-meshheading:7949151-Tumor Virus Infections,
pubmed-meshheading:7949151-Viral Matrix Proteins,
pubmed-meshheading:7949151-Virus Activation
|
| pubmed:year |
1994
|
| pubmed:articleTitle |
Interleukin-6 and Epstein-Barr virus induction by cyclosporine A: potential role in lymphoproliferative disease.
|
| pubmed:affiliation |
Laboratory of Immunovirology, Pediatric Research Center, University of Montréal, Quebéc, Canada.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|