The protective effect of interfering TLR9-IRF5 signaling pathway on the development of CVB3-induced myocarditis

Copyright © 2019. Published by Elsevier Inc.

Détails bibliographiques
Publié dans:Clinical immunology (Orlando, Fla.). - 1999. - 207(2019) vom: 15. Okt., Seite 24-35
Auteur principal: Nie, Shu (Auteur)
Autres auteurs: Dong, Boqi, Gao, Shuang, Zhou, Yan, Lu, Wenting, Fang, Mingli, Hua, Shucheng, Yu, Yongli, Wang, Liying
Format: Article en ligne
Langue:English
Publié: 2019
Accès à la collection:Clinical immunology (Orlando, Fla.)
Sujets:Journal Article Research Support, Non-U.S. Gov't Coxsackievirus B3 Interferon regulatory factor 5 Myocarditis Oligodeoxynucleotide Toll-like receptor 9 Cytokines Interferon Regulatory Factors Irf5 protein, mouse plus... Oligodeoxyribonucleotides Tlr9 protein, mouse Toll-Like Receptor 9
Description
Résumé:Copyright © 2019. Published by Elsevier Inc.
Since toll-like receptor 9 (TLR9) or interferon regulatory factor 5 (IRF5) was reported to be associated with the development of myocarditis, we wondered if the TLR9-IRF5 pathway could contribute to the development of coxsackievirus B3 (CVB3)-induced myocarditis. We detected signaling molecules of TLR9-IRF5 pathway in CVB3-infected patients and mice. The results showed that TLR9, IRF5 and its downstream molecules such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were significantly increased, and the increase was correlated with the severity of heart injury during CVB3 infection. In addition, we demonstrated that an AAAG ODN with IRF5 interfering activities significantly decreased the levels of the TLR9-IRF5 pathway molecules in hearts, spleens as well as white blood cells, and alleviated the myocarditis in CVB3-infected mice. The data suggest that interfering TLR9-IRF5 pathway could be an approach to treat CVB3-induced myocarditis
Description:Date Completed 18.05.2020
Date Revised 18.05.2020
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2019.07.002