Antagonism of Interleukin-17A ameliorates experimental hepatic fibrosis by restoring the IL-10/STAT3-suppressed autophagy in hepatocytes
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// Xiao-Wei Zhang 1 , Su Mi 1 , Zhe Li 1 , Ji-Chao Zhou 1 , Jing Xie 1 , Fang Hua 1 , Ke Li 2 , Bing Cui 1 , Xiao-Xi Lv 1 , Jiao-Jiao Yu 1 , Zhuo-Wei Hu 1 1 Molecular Immunology and Pharmacology Group, State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China 2 Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China Correspondence to: Zhuo-Wei Hu, email: huzhuowei@imm.ac.cn Keywords: cirrhosis, inflammation, liver injury, neutralizing antibody, p62 Received: August 23, 2016 Accepted: December 01, 2016 Published: December 27, 2016 ABSTRACT Interleukin-17A has been identified as a driver of hepatic stellate cell activation and plays a critical role in the pathogenesis of hepatic fibrosis. However, the underlining fibrosis-promoting mechanism of IL-17A is far from understood. Here we aimed to define whether hepatocytes directly respond to IL-17A stimulation and are associated with the development of hepatic fibrosis. The functional significance of IL-17A was evaluated in bile duct ligation (BDL) or thioacetamide (TAA) injection-induced mouse models of hepatic fibrosis. Human cirrhosis and control tissues were obtained from the patients with cirrhosis who received an open surgical repair process. Neutralizing IL-17A promoted the resolution of BDL or TAA-induced acute or chronic inflammation and fibrosis, resulted in a shift of the suppressive immune response in fibrotic liver toward a Th1-type immune response, and restored autophagy activity in both cholestatic and hepatotoxic liver injury induced fibrotic liver tissues, which was accompanied by a significant inhibition of STAT3 phosphorylation. Moreover, we found that IL-17A stimulated the concentration-and time-dependent phosphorylation of STAT3 in AML-12 liver cells. Blocking STAT3 with a specific inhibitor STATTIC or STAT3 siRNA protected from the IL-17A-induced autophagy suppression in AML-12 cells, indicating that STAT3 mediates IL-17A-suppressed autophagy. Administration of IL-10, which activated STAT3 and inhibited autophagy, reversed the therapeutic effect of IL-17A antagonism in vivo . Our study suggests that the IL-17A/STAT3 signaling pathway plays a crucial role in the pathogenesis of hepatic fibrosis through suppressing hepatocellular autophagy and that blocking this pathway may provide therapeutic benefits for the treatment of hepatic fibrosis.
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IL-4 and IL-13 are distinct but important inducers of fibrosis.
“the type 2-associated cytokines IL-4 and IL-13 have also emerged as distinct but important inducers of fibrosis”
From Fibrosis: from mechanisms to medicines (2020) · cites this paper as [128]
The type 2 cytokine fibrotic response is associated with a predominant eosinophil and M2-like macrophage infiltrate, rather than the neutrophil and M1-like monocyte/macrophage phenotype that characterizes the IL-1-IL-17A-TGF-β axis.
“Here, the fibrotic response is associated with a predominant eosinophil and M2-like macrophage infiltrate, rather than the neutrophil and M1-like monocyte/macrophage phenotype that characterizes the IL-1-IL-17A-TGF-β axis128”
From Fibrosis: from mechanisms to medicines (2020) · cites this paper as [128]
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- Authors
- Zhang, X.-W., Mi, S., Li, Z., Zhou, J.-C., Xie, J., Hua, F., Li, K., Cui, B., Lv, X.-X., Yu, J.-J., & Hu, Z.-W.
- Affiliations
- Molecular Immunology and Pharmacology Group, State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China
- Chinese Academy of Medical Sciences & Peking Union Medical College (CN)
- Venue
- Oncotarget
- Publisher
- Impact Journals, LLC
- Published
- 2016-12-27
- Volume
- 8
- Issue
- 6
- Pages
- 9922-9934
- ISSN
- 1949-2553 (ISSN-L)
- PMC
- PMC5354781
- OpenAlex
- W2567358604
- Cited by
- 48
- References
- 38
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 3 · 2023: 2 · 2022: 7 · 2021: 7 · 2020: 4 · 2019: 6 · 2018: 7 · 2017: 4
- FWCI
- 4.09
- Type
- journal article
- Language
- en
- Open access
- diamond
- doi.org
- Licence
- cc-by
- Locations
- Oncotarget (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (81400286, 81273529, 81530093)
- Peking Union Medical College
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Hepatology › Liver Diseases and Immunity
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Keywords
- liver fibrosis, autophagy, STAT3 phosphorylation, IL-10, hepatocytes, bile duct ligation, thioacetamide, liver cirrhosis, hepatic stellate cells, Th1 response, Stattic, p62, cholestatic liver injury, liver regeneration
- MeSH terms
- Animals, Autophagy, Cell Line, Cholestasis, Cyclic S-Oxides, Humans, Liver, Liver Cirrhosis, Experimental, Male, Mice, Inbred BALB C, Phosphorylation, Thioacetamide, Transfection, Signal Transduction, Interleukin-10, Th1 Cells, Interleukin-17, Hepatocytes, RNA Interference, STAT3 Transcription Factor, Chemical and Drug Induced Liver Injury, Antibodies, Neutralizing
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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