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CLPTM1L 是一个GPI-anchoring路径组件,是HCMV的目标

Inbal Kol¹, Ahmed Rishiq¹, Mevaseret Cohen¹

¹The Concern Foundation Laboratories at the Lautenberg Center for Immunology and Cancer Research, Institute for Medical Research Israel Canada, Hadassah-Hebrew University Medical Center , Jerusalem, Israel.

The Journal of cell biology

|June 30, 2023

概括

研究人员发现了一种新的途径组件,裂口口唇和 palatal 跨膜蛋白 1-like 蛋白 (CLPTM1L),参与定蛋白质到细胞膜. 人类细胞巨型病毒 (HCMV) 利用CLPTM1L在感染期间降低免疫相互作用蛋白质的调节.

科学领域:

分子生物学分子生物学
免疫学免疫学免疫学
病毒学病毒学

背景情况:

葡萄糖酸氨醇 (GPI) 定途径对于细胞发育和免疫反应至关重要.
与MHC I类多相关的A序列 (MICA) 是一种压力诱导的连接体,通常由人细胞巨核病毒 (HCMV) 降低调节,以逃避免疫检测.
流行的MICA*008等位基因使用未知途径进行GPI定.

研究的目的:

为了确定负责MICA*008定的非特征化的GPI定路径组件.
阐明HCMV在感染期间降低MICA*008的机制.
调查已识别的成分在其他GPI定蛋白的表达中的作用.

主要方法:

蛋白质的识别和表征.
使用HCMV.进行病毒感染测定.
西方涂抹和基因沉默技术用于评估蛋白质表达.
同免疫沉以研究蛋白质相互作用.

主要成果:

裂口唇跨膜蛋白1-类蛋白 (CLPTM1L) 被确定为GPI定途径的新型组件.
在感染期间,HCMV蛋白US9被证明可以通过CLPTM1L降低MICA*008的表达.
对一些GPI定蛋白质 (CD109,CD59,MELTF) 观察到CLPTM1L依赖的表达,但对其他蛋白质 (ULBP2,ULBP3) 没有观察到.
在HCMV感染期间,MELTF也被发现被US9通过CLPTM1L下调.
CLPTM1L的功能似乎取决于它与PIG-T的自由形式的相互作用,这是GPI转胺酶复合物的组成部分.
US9抑制了CLPTM1L-PIG-T相互作用,导致CLPTM1L依赖蛋白的下调.

结论:

CLPTM1L是GPI定途径的一个新发现的组件.
冠状病毒利用CLPTM1L降低关键的免疫相互作用蛋白质的调节,如MICA*008和MELTF.
HCMV蛋白US9针对CLPTM1L和PIG-T之间的相互作用,以破坏GPI定和逃避免疫监测.

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