Interleukin-17 contributes to the pathogenesis of autoimmune hepatitis through inducing hepatic interleukin-6 expression

Li Zhao, Yanli Tang, Zhengrui You, Qixia Wang, Shuwen Liang, Xiaofeng Han, Dekai Qiu, Jue Wei, Yuan Liu, Lei Shen, Xiaoyu Chen, Yanshen Peng, Zhiping Li, Xiong Ma

Research output: Contribution to journalArticlepeer-review

145 Scopus citations


T helper cells that produce IL-17 (Th17 cells) have recently been identified as the third distinct subset of effector T cells. Emerging data suggests that Th17 cells play an important role in the pathogenesis of many liver diseases by regulating innate immunity, adaptive immunity, and autoimmunity. In this study, we examine the role and mechanism of Th17 cells in the pathogenesis of autoimmune hepatitis (AIH). The serum levels of IL-17 and IL-23, as well as the frequency of IL-17+ cells in the liver, were significantly elevated in patients with AIH, compared to other chronic hepatitis and healthy controls. The hepatic expressions of IL-17, IL-23, ROR-γt, IL-6 and IL-1β in patients with AIH were also significantly increased and were associated with increased inflammation and fibrosis. IL-17 induces IL-6 expression via the MAPK signaling pathway in hepatocytes, which, in turn, may further stimulate Th17 cells and forms a positive feedback loop. In conclusion, Th17 cells are key effector T cells that regulate the pathogenesis of AIH, via induction of MAPK dependent hepatic IL-6 expression. Blocking the signaling pathway and interrupting the positive feedback loop are potential therapeutic targets for autoimmune hepatitis.

Original languageEnglish (US)
Article numbere18909
JournalPloS one
Issue number4
StatePublished - 2011
Externally publishedYes

ASJC Scopus subject areas

  • General


Dive into the research topics of 'Interleukin-17 contributes to the pathogenesis of autoimmune hepatitis through inducing hepatic interleukin-6 expression'. Together they form a unique fingerprint.

Cite this