Cardiac Fibroblasts Recruit Th17 Cells Infiltration Into Myocardium by Secreting CCL20 in CVB3-Induced acute Viral Myocarditis
| Autor: | Miao Yu, Jun Hu, Ming-Xin Zhu, Tong Zhao, Wei Liang, Shuang Wen, Huan-Huan Li, Qi Long, Min Wang, He-Ping Guo, Xiang Cheng, Yu-Hua Liao, Jing Yuan |
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| Jazyk: | angličtina |
| Rok vydání: | 2013 |
| Předmět: | |
| Zdroj: | Cellular Physiology and Biochemistry, Vol 32, Iss 5, Pp 1437-1450 (2013) |
| Druh dokumentu: | article |
| ISSN: | 1015-8987 1421-9778 |
| DOI: | 10.1159/000356581 |
| Popis: | Aims: Th17 cells contributed to myocardial inflammatory injury in acute viral myocarditis (AVMC), and the migration of these cells were mainly mediated by CCL20-secreting inflammatory cells. However, whether and how the resident cells such as cardiomyocytes and cardiac fibroblasts could mediate Th17 cell migration into the heart remains unclear in AVMC. Methods: The effect of CCL20 on the dynamic alterations of intracardiac Th17 cells and disease severity were investigated through the neutralization of CCL20 in AVMC mice. The key cells releasing CCL20 in the heart and the effects of CCL20-secreting cells on Th17 cell arrest, migration and differentiation were detected in vitro. Results: Neutralization of CCL20 efficiently repressed the myocardial inflammation along with the reduction of Th17 cell infiltrations in the course of AVMC. In vitro, after stimulations of TNF-α, IL-1β and IL-17, cardiac fibroblasts rather than cardiomyocytes could be dominantly induced for CCL20 production. CCL20-secreting cardiac fibroblasts boosted Th17 cell arrest on endothelium, and induce Th17 cell migration. However, CCL20 produced by cardiac fibroblasts had no effect on Th17 cell differentiation and IL-17 production. Conclusions: It firstly suggested that cardiac fibroblasts could recruit Th17 cells infiltration into myocardium by secreting CCL20 in AVMC. |
| Databáze: | Directory of Open Access Journals |
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