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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1 Pt 1
pubmed:dateCreated
1994-6-2
pubmed:abstractText
Cytomegalovirus infection, a common complication in immunosuppressed graft recipients, bears an adverse impact on graft survival. Cytomegalovirus enhances the expression of the monotypic determinants of the class I major histocompatibility complex molecule by the endothelium, possibly rendering the endothelial cells more immunogenic and prone to attack by the allogeneic lymphocytes. In the present study, we focused on the effect of cytomegalovirus on the endothelial cell expression of different class I genes, on the relation between the extent of endothelial cell infection and the class I effect, and on the time course of the class I changes induced by the cytomegalovirus infection. Cytomegalovirus infection of primary cultures of human umbilical vein endothelial cells augmented the expression of the A2, A3, and B7 class I major histocompatibility complex genes when compared with uninfected cells. beta 2 microglobulin upregulation by the infected cells paralleled the changes in specific class I expression; this effect was significant only after 7 days after infection. Double immunocytochemical staining and fluorescence-activated cell sorter analysis revealed that the class I enhancement was uniform throughout the umbilical vein endothelial cell monolayer and not restricted to the cells that expressed cytomegalovirus early or late antigens. Ultraviolet-inactivated supernatants from infected umbilical vein endothelial cell did not increase class I expression on uninfected cells. In conclusion, cytomegalovirus might affect graft survival by amplifying the changes in class I expression beyond the sites of viral replication.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1053-2498
pubmed:author
pubmed:issnType
Print
pubmed:volume
13
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
129-38
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed-meshheading:8167118-Antibody Specificity, pubmed-meshheading:8167118-Antigens, Viral, pubmed-meshheading:8167118-Cells, Cultured, pubmed-meshheading:8167118-Cytomegalovirus, pubmed-meshheading:8167118-Cytomegalovirus Infections, pubmed-meshheading:8167118-Cytoplasm, pubmed-meshheading:8167118-Endothelium, Vascular, pubmed-meshheading:8167118-Gene Amplification, pubmed-meshheading:8167118-Gene Expression Regulation, Viral, pubmed-meshheading:8167118-HLA-A2 Antigen, pubmed-meshheading:8167118-HLA-A3 Antigen, pubmed-meshheading:8167118-HLA-B7 Antigen, pubmed-meshheading:8167118-Histocompatibility Antigens Class I, pubmed-meshheading:8167118-Humans, pubmed-meshheading:8167118-Ultraviolet Rays, pubmed-meshheading:8167118-Up-Regulation, pubmed-meshheading:8167118-Virus Replication, pubmed-meshheading:8167118-Virus Shedding, pubmed-meshheading:8167118-beta 2-Microglobulin
pubmed:articleTitle
Cytomegalovirus infection amplifies class I major histocompatibility complex expression on cultured human endothelial cells.
pubmed:affiliation
Transplantation Immunology Laboratory, Instituto do Coração, University of São Paulo, School of Medicine, Brazil.
pubmed:publicationType
Journal Article