Cargando…
Interleukin-17 Contributes to the Pathogenesis of Autoimmune Hepatitis through Inducing Hepatic Interleukin-6 Expression
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....
Autores principales: | , , , , , , , , , , , , , |
---|---|
Formato: | Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2011
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3079758/ https://www.ncbi.nlm.nih.gov/pubmed/21526159 http://dx.doi.org/10.1371/journal.pone.0018909 |
_version_ | 1782202062775255040 |
---|---|
author | Zhao, Li Tang, Yanli You, Zhengrui Wang, Qixia Liang, Shuwen Han, Xiaofeng Qiu, Dekai Wei, Jue Liu, Yuan Shen, Lei Chen, Xiaoyu Peng, Yanshen Li, Zhiping Ma, Xiong |
author_facet | Zhao, Li Tang, Yanli You, Zhengrui Wang, Qixia Liang, Shuwen Han, Xiaofeng Qiu, Dekai Wei, Jue Liu, Yuan Shen, Lei Chen, Xiaoyu Peng, Yanshen Li, Zhiping Ma, Xiong |
author_sort | Zhao, Li |
collection | PubMed |
description | 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. |
format | Text |
id | pubmed-3079758 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-30797582011-04-27 Interleukin-17 Contributes to the Pathogenesis of Autoimmune Hepatitis through Inducing Hepatic Interleukin-6 Expression Zhao, Li Tang, Yanli You, Zhengrui Wang, Qixia Liang, Shuwen Han, Xiaofeng Qiu, Dekai Wei, Jue Liu, Yuan Shen, Lei Chen, Xiaoyu Peng, Yanshen Li, Zhiping Ma, Xiong PLoS One Research Article 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. Public Library of Science 2011-04-19 /pmc/articles/PMC3079758/ /pubmed/21526159 http://dx.doi.org/10.1371/journal.pone.0018909 Text en Zhao et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Zhao, Li Tang, Yanli You, Zhengrui Wang, Qixia Liang, Shuwen Han, Xiaofeng Qiu, Dekai Wei, Jue Liu, Yuan Shen, Lei Chen, Xiaoyu Peng, Yanshen Li, Zhiping Ma, Xiong Interleukin-17 Contributes to the Pathogenesis of Autoimmune Hepatitis through Inducing Hepatic Interleukin-6 Expression |
title | Interleukin-17 Contributes to the Pathogenesis of Autoimmune Hepatitis through Inducing Hepatic Interleukin-6 Expression |
title_full | Interleukin-17 Contributes to the Pathogenesis of Autoimmune Hepatitis through Inducing Hepatic Interleukin-6 Expression |
title_fullStr | Interleukin-17 Contributes to the Pathogenesis of Autoimmune Hepatitis through Inducing Hepatic Interleukin-6 Expression |
title_full_unstemmed | Interleukin-17 Contributes to the Pathogenesis of Autoimmune Hepatitis through Inducing Hepatic Interleukin-6 Expression |
title_short | Interleukin-17 Contributes to the Pathogenesis of Autoimmune Hepatitis through Inducing Hepatic Interleukin-6 Expression |
title_sort | interleukin-17 contributes to the pathogenesis of autoimmune hepatitis through inducing hepatic interleukin-6 expression |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3079758/ https://www.ncbi.nlm.nih.gov/pubmed/21526159 http://dx.doi.org/10.1371/journal.pone.0018909 |
work_keys_str_mv | AT zhaoli interleukin17contributestothepathogenesisofautoimmunehepatitisthroughinducinghepaticinterleukin6expression AT tangyanli interleukin17contributestothepathogenesisofautoimmunehepatitisthroughinducinghepaticinterleukin6expression AT youzhengrui interleukin17contributestothepathogenesisofautoimmunehepatitisthroughinducinghepaticinterleukin6expression AT wangqixia interleukin17contributestothepathogenesisofautoimmunehepatitisthroughinducinghepaticinterleukin6expression AT liangshuwen interleukin17contributestothepathogenesisofautoimmunehepatitisthroughinducinghepaticinterleukin6expression AT hanxiaofeng interleukin17contributestothepathogenesisofautoimmunehepatitisthroughinducinghepaticinterleukin6expression AT qiudekai interleukin17contributestothepathogenesisofautoimmunehepatitisthroughinducinghepaticinterleukin6expression AT weijue interleukin17contributestothepathogenesisofautoimmunehepatitisthroughinducinghepaticinterleukin6expression AT liuyuan interleukin17contributestothepathogenesisofautoimmunehepatitisthroughinducinghepaticinterleukin6expression AT shenlei interleukin17contributestothepathogenesisofautoimmunehepatitisthroughinducinghepaticinterleukin6expression AT chenxiaoyu interleukin17contributestothepathogenesisofautoimmunehepatitisthroughinducinghepaticinterleukin6expression AT pengyanshen interleukin17contributestothepathogenesisofautoimmunehepatitisthroughinducinghepaticinterleukin6expression AT lizhiping interleukin17contributestothepathogenesisofautoimmunehepatitisthroughinducinghepaticinterleukin6expression AT maxiong interleukin17contributestothepathogenesisofautoimmunehepatitisthroughinducinghepaticinterleukin6expression |