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NK cells induce MHC class II molecules on the surface of allogeneic endothelial cells in an adhesion-dependent, IFN-γ-independent manner. Here, we demonstrate that NK cells induce HLA-DR on the surface of a mutant cell line that is defective in IFN-γ-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-DRα mRNA expression is also CIITA-independent. The Janus kinase-1-deficient cell line U4A expresses HLA-DRα mRNA in response to NK cell activation, and HLA-DRα promoter constructs transfected into these cells are induced by NK cells but not IFN-γ. These data indicate that the IFN-γ-independent component of the target cell HLA-DR expression induced by lymphocyte adhesion uses a signaling pathway that is distinct from the IFN-γ-dependent mechanism and also suggest that CIITA is not required.
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Collinge et al. (1998) studied this question.
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