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pubmed-article:9712019pubmed:abstractTextNK cells induce MHC class II molecules on the surface of allogeneic endothelial cells in an adhesion-dependent, IFN-gamma-independent manner. Here, we demonstrate that NK cells induce HLA-DR on the surface of a mutant cell line that is defective in IFN-gamma-induced MHC class II expression. RNA analysis in these cells and in a cell line that is defective in class II transactivator (CIITA) demonstrates that NK cell-induced HLA-DR alpha mRNA expression is also CIITA-independent. The Janus kinase-1-deficient cell line U4A expresses HLA-DR alpha mRNA in response to NK cell activation, and HLA-DR alpha promoter constructs transfected into these cells are induced by NK cells but not IFN-gamma. These data indicate that the IFN-gamma-independent component of the target cell HLA-DR expression induced by lymphocyte adhesion uses a signaling pathway that is distinct from the IFN-gamma-dependent mechanism and also suggest that CIITA is not required.lld:pubmed
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pubmed-article:9712019pubmed:dateRevised2008-11-21lld:pubmed
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pubmed-article:9712019pubmed:articleTitleClass II transactivator-independent endothelial cell MHC class II gene activation induced by lymphocyte adhesion.lld:pubmed
pubmed-article:9712019pubmed:affiliationDivision of Cardiovascular Medicine, Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, CT 06536, USA. mark.collinge@yale.edulld:pubmed
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