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CUTTING EDGE |
*
Molecular Cardiobiology Program, Division of Cardiovascular Medicine, and the Raymond and Beverly Sackler Foundation Laboratory, Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, CT 06536; and
Unit of Clinical Immunology, Department of Biological and Technical Research, San Raffaele Scientific Institute, Milan, Italy
NK cells induce MHC class II molecules on the surface of
allogeneic endothelial cells in an adhesion-dependent,
IFN-
-independent manner. Here, we demonstrate that NK cells induce
HLA-DR on the surface of a mutant cell line that is defective in
IFN--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
mRNA expression is also
CIITA-independent. The Janus kinase-1-deficient cell line U4A expresses
HLA-DR mRNA in response to NK cell activation, and HLA-DR
promoter constructs transfected into these cells are induced by NK
cells but not IFN-. These data indicate that the IFN--independent
component of the target cell HLA-DR expression induced by lymphocyte
adhesion uses a signaling pathway that is distinct from the
IFN--dependent mechanism and also suggest that CIITA is not
required.
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