Cited by 504IL-33, ST2, and ILC PathwaysLiver physiology and pathologyLiver Disease Diagnosis and Treatment

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Interleukin-33-Dependent Innate Lymphoid Cells Mediate Hepatic Fibrosis

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Mchedlidze, Tamar, Waldner, Maximilian, Zopf, Steffen, Walker, Jennifer, Rankin, Andrew L., Schuchmann, Marcus, Voehringer, David, McKenzie, Andrew N.J., Neurath, Markus F., Pflanz, Stefan, Wirtz, Stefan·2013·Immunity

DOI 10.1016/j.immuni.2013.07.018PMC PMC4172965

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Abstract

Liver fibrosis is a consequence of chronic liver diseases and thus a major cause of mortality and morbidity. Clinical evidence and animal studies suggest that local tissue homeostasis is disturbed due to immunological responses to chronic hepatocellular stress. Poorly defined stress-associated inflammatory networks are thought to mediate gradual accumulation of extracellular-matrix components, ultimately leading to fibrosis and liver failure. Here we have reported that hepatic expression of interleukin-33 (IL-33) was both required and sufficient for severe hepatic fibrosis in vivo. We have demonstrated that IL-33's profibrotic effects related to activation and expansion of liver resident innate lymphoid cells (ILC2). We identified ILC2-derived IL-13, acting through type-II IL-4 receptor-dependent signaling via the transcription factor STAT6 and hepatic stellate-cell activation, as a critical downstream cytokine of IL-33-dependent pathologic tissue remodeling and fibrosis. Our data reveal key immunological networks implicated in hepatic fibrosis and support the concept of modulation of IL-33 bioactivity for therapeutic purposes.

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Authors: Mchedlidze, T., Waldner, M., Zopf, S., Walker, J., Rankin, A. L., Schuchmann, M., Voehringer, D., McKenzie, A. N. J., Neurath, M. F., Pflanz, S., & Wirtz, S.
Affiliations: Friedrich-Alexander-Universität Erlangen-Nürnberg (DE)
MRC Laboratory of Molecular Biology (GB)
Merck & Co., Inc., Rahway, NJ, USA (United States) (US)
Johannes Gutenberg University Mainz (DE)
Corresponding author: Wirtz, Stefan
ORCID: Waldner, Maximilian
Walker, Jennifer
Voehringer, David
McKenzie, Andrew N.J.
Neurath, Markus F.
Wirtz, Stefan
Venue: Immunity
Publisher: Elsevier BV
Published: 2013-08
Volume: 39
Issue: 2
Pages: 357-371
ISSN: 1074-7613 (ISSN-L)
DOI: 10.1016/j.immuni.2013.07.018
PMC: PMC4172965
OpenAlex: W1997883939
Cited by: 502
References: 54
Citations by year: 2026: 13 · 2025: 33 · 2024: 30 · 2023: 33 · 2022: 35 · 2021: 37 · 2020: 46 · 2019: 43 · 2018: 48 · 2017: 50 · 2016: 47 · 2015: 47 · 2014: 35 · 2013: 4
FWCI: 24.68
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 386 d)
Locations: Immunity (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Topics: Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Health Sciences › Medicine › Hepatology › Liver Disease Diagnosis and Treatment
Keywords: IL-33, liver fibrosis, innate lymphoid cells, ILC2, IL-13, STAT6, hepatic stellate cells, extracellular matrix remodeling, liver inflammation, chronic liver disease
MeSH terms: Interleukin-33, Animals, Cells, Cultured, Inflammation, Interleukins, Liver, Liver Cirrhosis, Lymphocyte Activation, Lymphocytes, Mice, Inbred BALB C, Mice, Inbred C57BL, Signal Transduction, Mice, Knockout, Interleukin-13, Adoptive Transfer, Cell Proliferation, STAT6 Transcription Factor, Mice, Receptors, Interleukin-4, Type II, Hepatic Stellate Cells

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Interleukin-33-Dependent Innate Lymphoid Cells Mediate Hepatic Fibrosis

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