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Several cell types are considered to be effector cells in bile duct injury in rhesus rotavirus(RRV)-induced experimental biliary atresia(BA).Here,we identified an increased T helper 17(Th17)cell population in a BA mode.By depleting the Th17 cells,the BA symptoms(onset of jaundice,pale acholic stools and retarded growth)were attenuated and the survival rate was improved.Furthermore,we found that in mice with BA,the percentage of CD4+CD25highFoxp3+T regulatory(Treg)cells decreased along with the increased percentage of Th17 cells.However,the absolute numbers of Treg and Th17 cells were both increased relative to normal mice.The proportion of Th17 cells at 7 days post-infection was decreased if Treg cells isolated from normal adult mice,but not Treg cells from the livers of mice with BA,were intraperitoneally transferred on day 5 of life.In vitro experiments also showed that Treg cells from mice with BA had a diminished suppressive effect on Th17 cell generation.To determine the mechanisms,we investigated the production of cytokines in the liver.The level of IL-6,which has been shown to be abundantly secreted by activated dendritic cells(DCs),was remarkably elevated.Accordingly,when we injected anti-IL-6 antibody 24 h post-infection,we observed that the pro-inflammatory response was dampened and that disease progression was suppressed.Importantly,in a Treg/Th17 cell suppression assay,IL-6 was demonstrated to paralyze the Treg cells suppressive effect on Th17 cells and eventually the unrestrained increase in Th17 cells contributed to bile duct injury.In conclusion,the DC-regulated Treg-Th17 axis,probably in conjunction with other effector T cells,aggravates progressive inflammatory injury at the time of ductal obstruction.