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罗塔病毒感染通过通过ERAD-蛋白酶体通路降解β2M来抑制细胞表面的SLA-I表达

Zhaoyang Jing¹, Ling Wu¹, Yudi Pan¹

¹State Key Laboratory for Animal Disease Control and Prevention, Harbin Veterinary Research Institute, Harbin, People's Republic of China.

Veterinary microbiology

|March 8, 2024

概括

A组罗塔病毒 (RVA) 感染通过ERAD-蛋白酶体通路触发其降解来降低β2-微型球蛋白 (β2M) 蛋白质水平. 这导致细胞表面的猪白细胞抗原I类 (SLA-I) 减少,有助于病毒免疫逃逸.

科学领域:

病毒学病毒学
免疫学免疫学免疫学
细胞生物学细胞生物学

背景情况:

A组罗塔病毒 (RVA) 是婴儿和小猪腹的重要原因.
贝塔2-微球蛋白 (β2M) 对于主要基因相容性复合物I类 (MHC-I) 表面表达至关重要,呈现病毒抗原.
在猪中,MHC-I被称为猪白细胞抗原I类 (SLA-I).

研究的目的:

研究RVA感染对猪肠上皮细胞 (IPEC-J2) 和MA-104细胞中β2M表达的影响.
阐明RVA影响β2M水平的机制.
为了确定RVA诱导的β2M下调对SLA-I表面表达的影响.

主要方法:

在IPEC-J2和MA-104细胞系的RVA感染.
对β2M mRNA和蛋白质水平的分析.
在内质网膜 (ER) 中研究β2M聚合和泛化.
评估ER相关降解 (ERAD) 和蛋白酶体通路参与.
细胞表面SLA-I表达的测量.

主要成果:

在两种细胞类型中,RVA感染显著降低了β2M蛋白表达,但并没有降低B2MmRNA水平.
RVA感染诱导了ER中的β2M聚合,并增加了其K48结合的无化,将其定位为ERAD-蛋白酶体降解.
RVA感染显著降低了表面SLA-I水平.
过度表达β2M恢复了SLA-I表面表达.

结论:

RVA感染通过ERAD-蛋白酶体通路降解β2M.
因此,β2M的减少会影响SLA-I表面表达.
这种机制通过限制病毒抗原呈现,有助于RVA诱导的免疫逃脱.

关键词:

在ERAD-蛋白酶体通路中,与K48相关的无处不在化.RVA RVA 是一个值得信赖的数字.这就是SLA-I.β 2M 2M 的时间.

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