生物
免疫系统
肌动蛋白细胞骨架
细胞生物学
细胞骨架
肌动蛋白
免疫突触
人巨细胞病毒
细胞毒性T细胞
病毒学
细胞
免疫学
T细胞
病毒
遗传学
体外
T细胞受体
作者
Richard J. Stanton,Virginie Prod’homme,Marco A. Purbhoo,Melanie Moore,Rebecca J. Aicheler,Marcus Heinzmann,Susanne M. Bailer,Jürgen Haas,Robin Antrobus,Michael P. Weekes,Paul J. Lehner,Bořivoj Vojtěšek,Kelly L. Miners,Stephen Man,Gavin S. Wilkie,Andrew J. Davison,Eddie C. Y. Wang,Peter Tomašec,Gavin W. G. Wilkinson
标识
DOI:10.1016/j.chom.2014.07.005
摘要
Immune evasion genes help human cytomegalovirus (HCMV) establish lifelong persistence. Without immune pressure, laboratory-adapted HCMV strains have undergone genetic alterations. Among these, the deletion of the UL/b' domain is associated with loss of virulence. In a screen of UL/b', we identified pUL135 as a protein responsible for the characteristic cytopathic effect of clinical HCMV strains that also protected from natural killer (NK) and T cell attack. pUL135 interacted directly with abl interactor 1 (ABI1) and ABI2 to recruit the WAVE2 regulatory complex to the plasma membrane, remodel the actin cytoskeleton and dramatically reduce the efficiency of immune synapse (IS) formation. An intimate association between F-actin filaments in target cells and the IS was dispelled by pUL135 expression. Thus, F-actin in target cells plays a critical role in synaptogenesis, and this can be exploited by pathogens to protect against cytotoxic immune effector cells. An independent interaction between pUL135 and talin disrupted cell contacts with the extracellular matrix.
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