foxp3和il23il17a信号通路对慢性乙肝的作用分析word格式论文.docxVIP

sharply in the first 12 weeks, but then began to rise slowly. IL-23/IL-17A pathway-related proinflammatory cytokines were also found to be significantly increased in patients’ liver tissues, as compared to HCs. The high expression of IL-23/IL-17A pathway was highly correlated with the serum concentration of HBsAg if only HBsAg concentration was higher than 1×104 IU/ml. Along with the 52 weeks’ treatment of Telbivudine, the expression of IL-23/IL-17A decreased slowly and continuously. Moreover, FOXP3 expression was strikingly correlated with the productions of these cytokines in liver tissues of CHB patients.Conclusion The expression of FOXP3 is significantly increased in PBMCs and liver tissue of CHB patients, and then decrease dramatically following the treatment of Telbivudine. These results indicate that FOXP3 expression is likely to restrain the effective antiviral immunity so as to support the established residence of HBV. IL-23/IL-17A pathway activity increases in the patients of CHB and ACLF and then decreases continually with the 52 weeks’ treatment of Telbivudine, indicates that the IL-23/IL-17A pathway, rather than IL-17A alone, is involved in the pathological process of hepatitis B infection. The closely-correlated increase of FOXP3 and IL-23/IL-17A pathway activity in HBV-infected livers suggests that the proinflammatory IL-23/IL-17A pathway have not been effectively suppressed by the host immune machinery, such as Treg cells. However, the treatment of Telbivudine may restore Treg’s suppression on the IL-23/IL-17A pathway following the reduction of HBsAg by Telbivudine. Future studies will address the precise in vivo mechanism of the reciprocal regulation between FOXP3 and the IL-23/IL-17A pathway, and will contribute to the development of effective therapies to clear HBV from CHB patients.Key words: FOXP3; Treg cells; Th17; IL-23; IL-17A; Hepatitis B英文缩写一览表英文缩写英文全称中文对照ACLFacute on chronic liver failure慢性乙肝急性发作ALTalanine transaminase丙氨酸氨基转移酶APCallophyco