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一种真菌细菌蛋白质的宿主介导的泛素化抑制免疫力

Lin Wang¹, Juehui Wu^1,2, Jun Li³

¹Shanghai Key Laboratory of Tuberculosis, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.

|January 17, 2020

概括

结核菌利用宿主ANAPC2蛋白与其Rv0222蛋白结合,抑制宿主免疫反应. 这种相互作用对M.结核病的毒性至关重要,并为免疫调节剂提供了新的点.

科学领域:

免疫学
微生物学
分子生物学

背景情况:

结核菌 (M. tuberculosis) 是一种细胞内病原体,可以操纵宿主免疫信号.
细菌病原体经常利用宿主无处不在的系统来产生病原体.
宿主在M.结核病蛋白调节中的作用以前是未知的.

研究的目的:

调查宿主无化是否调节M.结核病蛋白.
阐明结核菌干扰宿主免疫信号的机制.
确定针对M.结核的新型免疫调节剂的潜在目标.

主要方法:

共同免疫沉以检测宿主和细菌蛋白之间的相互作用.
用于识别泛素链接类型的泛素化试验.
短发针RNA (shRNA) 抑制宿主基因表达.
针对位点的突变发生,以研究特定的无处不在位点的作用.
鼠感染模型以评估毒性.

主要成果:

主体E3无酸酶ANAPC2与M.结核病蛋白Rv0222发生相互作用.
ANAPC2将氨酸11链接到Rv0222,抑制促炎细胞因子的表达.
抑制 ANAPC2 或突变 Rv0222 无处可见部位会消除这种抑制并降低毒性.
通过Rv0222的化,SHP1可以更容易地被TRAF6吸收,从而抑制TRAF6的激活.

结论:

结核菌利用宿主ANAPC2介导的Rv0222的无化来抑制宿主免疫力.
这种机制涉及通过SHP1招募抑制TRAF6激活.
这些发现揭示了一种新的免疫逃避策略和结核病的潜在治疗点.

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