1. Aberrant PD-1 ligand expression contributes to the myocardial inflammatory injury caused by Coxsackievirus B infection.
- Author
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Wang, Tianying, Chen, Shuang, Wang, Xueqing, Huang, Yike, Qiu, Jianfa, Fei, Yanru, Chaulagain, Anita, Chen, Yang, Wang, Yan, Lin, Lexun, Yan, Biying, Wang, Ying, Wang, Wei, Zhao, Wenran, and Zhong, Zhaohua
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COXSACKIEVIRUS diseases , *PROGRAMMED cell death 1 receptors , *APOPTOSIS , *WOUNDS & injuries , *CARRIER proteins , *THERAPEUTICS - Abstract
Coxsackievirus group B (CVB) is considered as one of the most common pathogens of human viral myocarditis. CVB-induced myocarditis is mainly characterized by the persistence of the virus infection and immune-mediated inflammatory injury. Costimulatory signals are crucial for the activation of adaptive immunity. Our data reveal that the CVB type 3 (CVB3) infection altered the expression profile of costimulatory molecules in host cells. CVB3 infection caused the decrease of PD-1 ligand expression, partially due to the cleavage of AU-rich element binding protein AUF1 by the viral protease 3Cpro, leading to the exacerbated inflammatory injury of the myocardium. Moreover, systemic PD-L1 treatment, which augmented the apoptosis of proliferating lymphocytes, alleviated myocardial inflammatory injury. Our findings suggest that PD1-pathway can be a potential immunologic therapeutic target for CVB-induced myocarditis. • Coxsackievirus B3 infection causes costimulatory molecules profile changes. • Coxsackievirus B3 induces decrease of programmed cell death 1 ligands. • Treatment with programmed cell death ligand recombinant Ig could relieve myocardial inflammatory injury. [ABSTRACT FROM AUTHOR]
- Published
- 2019
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