Collinge M, Pardi R, Bender J R
Division of Cardiovascular Medicine, Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, CT 06536, USA.
J Immunol. 1998 Aug 15;161(4):1589-93.
NK 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.
自然杀伤（NK）细胞以黏附依赖、γ干扰素非依赖的方式诱导同种异体内皮细胞表面的主要组织相容性复合体（MHC）Ⅱ类分子。在此，我们证明NK细胞可在γ干扰素诱导的MHCⅡ类表达存在缺陷的突变细胞系表面诱导人类白细胞抗原-DR（HLA-DR）。对这些细胞以及Ⅱ类反式激活因子（CIITA）存在缺陷的细胞系进行RNA分析表明，NK细胞诱导的HLA-DRα mRNA表达也是CIITA非依赖的。Janus激酶-1缺陷的细胞系U4A在NK细胞激活后表达HLA-DRα mRNA，转染至这些细胞中的HLA-DRα启动子构建体可被NK细胞而非γ干扰素诱导。这些数据表明，淋巴细胞黏附诱导的靶细胞HLA-DR表达的γ干扰素非依赖成分使用的信号通路不同于γ干扰素依赖机制，也提示不需要CIITA。
