title: Cardiac fibroblasts recruit Th17 cells infiltration into myocardium by secreting CCL20 in CVB3-induced acute viral myocarditis.
abstract: OBJECTIVE
  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.
authors.forename: Miao
authors.initials: M
authors.lastname: Yu
authors.forename: Jun
authors.initials: J
authors.lastname: Hu
authors.forename: Ming-Xin
authors.initials: MX
authors.lastname: Zhu
authors.forename: Tong
authors.initials: T
authors.lastname: Zhao
authors.forename: Wei
authors.initials: W
authors.lastname: Liang
authors.forename: Shuang
authors.initials: S
authors.lastname: Wen
authors.forename: Huan-Huan
authors.initials: HH
authors.lastname: Li
authors.forename: Qi
authors.initials: Q
authors.lastname: Long
authors.forename: Min
authors.initials: M
authors.lastname: Wang
authors.forename: He-Ping
authors.initials: HP
authors.lastname: Guo
authors.forename: Xiang
authors.initials: X
authors.lastname: Cheng
authors.forename: Yu-Hua
authors.initials: YH
authors.lastname: Liao
authors.forename: Jing
authors.initials: J
authors.lastname: Yuan
mesh_terms: D000208:Acute Disease; D000818:Animals; D002454:Cell Differentiation; D054418:Chemokine CCL20 / Q000378:metabolism*; D003384:Coxsackievirus Infections / Q000378:metabolism / Q000473:pathology; D029822:Enterovirus B, Human / Q000472:pathogenicity; D005347:Fibroblasts / Q000378:metabolism* / Q000821:virology; D006321:Heart / Q000821:virology; D006801:Humans; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009205:Myocarditis / Q000378:metabolism / Q000473:pathology* / Q000821:virology; D009206:Myocardium / Q000166:cytology / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000821:virology; D058504:Th17 Cells / Q000378:metabolism / Q000473:pathology* / Q000821:virology
chemical_list: C493447:CCL20 protein, mouse; D054418:Chemokine CCL20