免疫压迫阵列揭示葡萄膜黑色素瘤中的免疫逃逸和生存机制。
Immune oppression array elucidating immune escape and survival mechanisms in uveal melanoma.
作者信息
Hou Fang, Huang Qi-Ming, Hu Dan-Ning, Jonas Jost B, Wei Wen-Bin
机构信息
Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing Ophthalmology and Visual Science Key Lab, Beijing 100730, China.
Departments of Ophthalmology and Pathology, New York Eye and Ear Infirmary of Mount Sinai, 310 E.14th St., NY 10003, USA.
出版信息
Int J Ophthalmol. 2016 Dec 18;9(12):1701-1712. doi: 10.18240/ijo.2016.12.01. eCollection 2016.
AIM
To examine the genetic profile of primary uveal melanoma (UM) as compared to UM in immune escape.
METHODS
Dendritic cells (DC) loaded with lysates of UM cells of high metastatic potential were used to stimulate CTLs(CTLs). When CTLs co-cultured with the UM cells, most UM cells could be eliminated. Survival UM cells grew slowly and were considered to be survival variants and examined by a microarray analysis. These differential genes were analyzed further with Venn Diagrams and functions related to immune escape. We additionally examined transcriptional changes of manually selected survival variants of UM cells and of clinical UM samples by quantitative real-time polymerase chain reaction (qRT-PCR), and analyzed the correlation of these expressions and patients' survival.
RESULTS
Gene expression analyses revealed a marked up-regulation of and and a significant down-regulation of , and . The expression of these genes in the relapsed UM was significantly greater than those in primary UM. UM patients with overexpression of these genes had a shorter survival period as compared with those of their underexpression.
CONCLUSION
Gene expression, in particular of and , differed between primary UM cells and survival variants of UM cells.
目的
对比原发性葡萄膜黑色素瘤（UM）与处于免疫逃逸状态的UM的基因图谱。
方法
用负载高转移潜能UM细胞裂解物的树突状细胞（DC）刺激细胞毒性T淋巴细胞（CTL）。当CTL与UM细胞共培养时，大多数UM细胞可被清除。存活的UM细胞生长缓慢，被视为存活变异体，并通过微阵列分析进行检测。用维恩图和与免疫逃逸相关的功能对这些差异基因进行进一步分析。我们还通过定量实时聚合酶链反应（qRT-PCR）检测了手动选择的UM细胞存活变异体和临床UM样本的转录变化，并分析了这些表达与患者生存的相关性。
结果
基因表达分析显示，[具体基因1]和[具体基因2]显著上调，而[具体基因3]、[具体基因4]和[具体基因5]显著下调。这些基因在复发性UM中的表达明显高于原发性UM。与基因低表达的UM患者相比，这些基因过度表达的UM患者生存期较短。
结论
原发性UM细胞与UM细胞存活变异体之间的基因表达存在差异，尤其是[具体基因1]和[具体基因2]。
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