Aberrant PD-1 ligand expression contributes to the myocardial inflammatory injury caused by Coxsackievirus B infection.


Journal

Antiviral research
ISSN: 1872-9096
Titre abrégé: Antiviral Res
Pays: Netherlands
ID NLM: 8109699

Informations de publication

Date de publication:
06 2019
Historique:
received: 31 10 2018
revised: 14 03 2019
accepted: 16 03 2019
pubmed: 25 3 2019
medline: 15 5 2020
entrez: 25 3 2019
Statut: ppublish

Résumé

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 3C

Identifiants

pubmed: 30904424
pii: S0166-3542(18)30663-6
doi: 10.1016/j.antiviral.2019.03.007
pii:
doi:

Substances chimiques

B7-H1 Antigen 0
Cd274 protein, mouse 0
Pdcd1 protein, mouse 0
Programmed Cell Death 1 Ligand 2 Protein 0
Programmed Cell Death 1 Receptor 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1-10

Informations de copyright

Copyright © 2019 Elsevier B.V. All rights reserved.

Auteurs

Tianying Wang (T)

Department of Microbiology, Harbin Medical University, Harbin, China; Heilongjiang Key Laboratory of Immunity and Infection, Harbin, China.

Shuang Chen (S)

Department of Immunology, Harbin Medical University, Harbin, China; Heilongjiang Key Laboratory of Immunity and Infection, Harbin, China.

Xueqing Wang (X)

Department of Microbiology, Harbin Medical University, Harbin, China; Heilongjiang Key Laboratory of Immunity and Infection, Harbin, China; School of Medical and Health Sciences, Edith Cowan University, Perth, Australia.

Yike Huang (Y)

Department of Cell Biology, Harbin Medical University, Harbin, China.

Jianfa Qiu (J)

Department of Microbiology, Harbin Medical University, Harbin, China; Heilongjiang Key Laboratory of Immunity and Infection, Harbin, China.

Yanru Fei (Y)

Department of Microbiology, Harbin Medical University, Harbin, China; Heilongjiang Key Laboratory of Immunity and Infection, Harbin, China.

Anita Chaulagain (A)

Department of Microbiology, Harbin Medical University, Harbin, China; Heilongjiang Key Laboratory of Immunity and Infection, Harbin, China.

Yang Chen (Y)

Department of Microbiology, Harbin Medical University, Harbin, China; Heilongjiang Key Laboratory of Immunity and Infection, Harbin, China.

Yan Wang (Y)

Department of Microbiology, Harbin Medical University, Harbin, China; Heilongjiang Key Laboratory of Immunity and Infection, Harbin, China.

Lexun Lin (L)

Department of Microbiology, Harbin Medical University, Harbin, China; Heilongjiang Key Laboratory of Immunity and Infection, Harbin, China.

Biying Yan (B)

Department of Microbiology, Harbin Medical University, Harbin, China; Heilongjiang Key Laboratory of Immunity and Infection, Harbin, China.

Ying Wang (Y)

Department of Microbiology, Harbin Medical University, Harbin, China; Heilongjiang Key Laboratory of Immunity and Infection, Harbin, China.

Wei Wang (W)

School of Medical and Health Sciences, Edith Cowan University, Perth, Australia.

Wenran Zhao (W)

Department of Cell Biology, Harbin Medical University, Harbin, China. Electronic address: zhaowr@hrbmu.edu.cn.

Zhaohua Zhong (Z)

Department of Microbiology, Harbin Medical University, Harbin, China; Heilongjiang Key Laboratory of Immunity and Infection, Harbin, China. Electronic address: zhongzh@hrbmu.edu.cn.

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Classifications MeSH