Interferon-γ Up-Regulates Major-Histocompatibility-Complex Class I-Related Chain A Expression and Enhances Major-Histocompatibility-Complex Class I-Related Chain A-Mediated Cytolysis of Human Corneal Epithelium by Natural Killer Cells In Vitro

被引:3
作者
Hong, Jiaxu [1 ]
Shao, Tingting [1 ]
Sun, Xinghuai [1 ,2 ]
Li, Gang [1 ]
Xu, Jianjiang [1 ]
机构
[1] Fudan Univ, Sch Shanghai Med, Eye Ear Nose & Throat Hosp, Dept Ophthalmol, Shanghai 200031, Peoples R China
[2] Inst Brain Sci, State Key Lab Med Neurobiol, Shanghai, Peoples R China
基金
中国国家自然科学基金;
关键词
MHC-CLASS-I; DOWN-REGULATION; NKG2D; LIGANDS; MELANOMA; CYTOTOXICITY; MOLECULES; MECHANISM; VIRUSES; CANCER;
D O I
10.1089/jir.2011.0003
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Natural killer (NK) cells are important in the ocular surface innate response against viral and bacterial infection. Major-histocompatibility-complex class I-related chain A (MICA) antigens are ligands of natural killer group 2D, an activating or coactivating receptor expressed on NK cells. Recent studies demonstrated that interferon-gamma (IFN-gamma) could modulate MICA expression in tumor cells. However, little is known about MICA expression and regulation in human corneal epithelium. Our study assessed whether the proinflammatory cytokine, IFN-gamma, affects MICA expression in human corneal epithelium. We identified low levels of surface MICA expression in corneal epithelium using flow cytometry. IFN-gamma promoted surface MICA expression in corneal epithelium and increased soluble MICA levels in a dose-dependent manner. IFN-gamma also enhanced NK cell-mediated cytotoxicity against the corneal epithelium. Anti-MICA antibodies could further block this process. In summary, we describe a novel IFN-gamma function in the regulation of the innate response in ocular surfaces.
引用
收藏
页码:115 / 120
页数:6
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