Interleukin-17 Signaling in Inflammatory, Kupffer Cells, and Hepatic Stellate Cells Exacerbates Liver Fibrosis in Mice
Open accessAbstract
Background & aims Interleukin (IL)-17 signaling has been implicated in lung and skin fibrosis. We examined the role of IL-17 signaling in the pathogenesis of liver fibrosis in mice.Methods Using cholestatic and hepatotoxic models of liver injury, we compared the development of liver fibrosis in wild-type mice with that of IL-17RA(-/-) mice and of bone marrow chimeric mice devoid of IL-17 signaling in immune and Kupffer cells (IL-17RA(-/-) to wild-type and IL-17A(-/-) to wild-type mice) or liver resident cells (wild-type to IL-17RA(-/-) mice).Results In response to liver injury, levels of Il-17A and its receptor increased. IL-17A increased appeared to promote fibrosis by activating inflammatory and liver resident cells. IL-17 signaling facilitated production of IL-6, IL-1, and tumor necrosis factor-α by inflammatory cells and increased the expression of transforming growth factor-1, a fibrogenic cytokine. IL-17 directly induced production of collagen type I in hepatic stellate cells by activating the signal transducer and activator of transcription 3 (Stat3) signaling pathway. Mice devoid of Stat3 signaling in hepatic stellate cells (GFAPStat3(-/-) mice) were less susceptible to fibrosis. Furthermore, deletion of IL-23 from immune cells attenuated liver fibrosis, whereas deletion of IL-22 exacerbated fibrosis. Administration of IL-22 and IL-17E (IL-25, a negative regulator of IL-23) protected mice from bile duct ligation-induced liver fibrosis.Conclusions IL-17 induces liver fibrosis through multiple mechanisms in mice. Reagents that block these pathways might be developed as therapeutics for patients with cirrhosis.
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ILC2s (via IL-33), T cells (via IL-17), B cells (immunoglobulin independent), Tregs (via amphiregulin) and platelets have been suggested to directly promote HSC activation.
“Additionally, ILC2s (via IL-33), T cells (via IL-17), B cells (immunoglobulin independent), Tregs (via amphiregulin) and platelets have been suggested to directly promote HSC activation [197, 237, 242–245].”
From Inflammation and immunity in liver homeostasis and disease: a nexus of hepatocytes, nonparenchymal cells and immune cells (2025) · cites this paper as [197]
TGF-β induces IL-17A expression when produced concurrently with IL-1, IL-6, or TNF.
“TGF-β in turn induced the expression of IL-17A when produced concurrently with the pro-inflammatory cytokines IL-1, IL-6, or TNF110,121,122”
From Fibrosis: from mechanisms to medicines (2020) · cites this paper as [122]
Sustained activation of the NLRP3 inflammasome is associated with increased chemokine expression, recruitment of neutrophils and macrophages, and persistent production of IL-17A and TNF.
“sustained activation of the NLRP3 inflammasome is associated with increased chemokine expression, recruitment of neutrophils and macrophages, and persistent production of IL-17A and TNF122”
From Fibrosis: from mechanisms to medicines (2020) · cites this paper as [122]
Caspase-1, NLRP3 inflammasome, and NFkB are important upstream mediators contributing to activation of the IL-17A-TGF-β axis.
“Caspase-1, NOD, LRR and pyrin domain-containing (NLRP) 3 inflammasome, and NFkB were identified as important upstream mediators contributing to the activation of the IL-17A-TGF-β axis122”
From Fibrosis: from mechanisms to medicines (2020) · cites this paper as [122]
Activation of the pro-fibrotic TGF-β signaling pathway is driven by several collaborating mechanisms, with IL-17A playing a prominent role.
“Thus, activation of the pro-fibrotic TGF-β signaling pathway is driven by several collaborating mechanisms, with the pro-inflammatory cytokine IL-17A playing a prominent role.”
From Fibrosis: from mechanisms to medicines (2020) · cites this paper as [122]
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- Authors
- Meng, F., Wang, K., Aoyama, T., Grivennikov, S. I., Paik, Y., Scholten, D., Cong, M., Iwaisako, K., Liu, X., Zhang, M., Österreicher, C. H., Stickel, F., Ley, K., Brenner, D. A., & Kisseleva, T.
- Affiliations
- Shandong University (CN)
- University of California San Diego (US)
- Kyoto University (JP)
- University Hospital of Bern (CH)
- La Jolla Institute for Immunology (US)
- Corresponding author
- Kisseleva, Tatiana
- ORCID
- Venue
- Gastroenterology
- Publisher
- Elsevier BV
- Published
- 2012-09
- Volume
- 143
- Issue
- 3
- Pages
- 765-776.e3
- ISSN
- 0016-5085 (ISSN-L)
- PMC
- PMC3635475
- OpenAlex
- W2005119615
- Cited by
- 711
- References
- 34
- Citations by year
- 2026: 47 · 2025: 57 · 2024: 53 · 2023: 64 · 2022: 63 · 2021: 58 · 2020: 54 · 2019: 44 · 2018: 50 · 2017: 36 · 2016: 46 · 2015: 48 · 2014: 42 · 2013: 42 · 2012: 7
- FWCI
- 28.20
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Gastroenterology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Bern Open Repository and Information System (University of Bern) (submittedVersion)
- RWTH Publications (RWTH Aachen) (submittedVersion)
- Funders
- National Institutes of Health (GM41804, AA15055, DK72237, AI077780)
- Shandong Province Science and Technology Plan (2006GG2202042)
- Key Project of Chinese Ministry of Science and Technology (2008ZX10002-007)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Hepatology › Liver Diseases and Immunity
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
- Keywords
- IL-17, liver fibrosis, Kupffer cells, hepatic stellate cells, IL-17RA, STAT3 signaling, IL-23, IL-22, cholestatic liver injury, bile duct ligation, type I collagen, TGF-beta, interleukin-6, TNF-α, liver cirrhosis
- MeSH terms
- Interleukin-22, Animals, Bile Ducts, Carbon Tetrachloride, Cell Line, Gene Expression Regulation, Genotype, Humans, Interleukin-1, Interleukins, Kupffer Cells, Ligation, Liver, Liver Cirrhosis, Alcoholic, Liver Cirrhosis, Experimental, Mice, Inbred C57BL, Phenotype, Time Factors, Tumor Necrosis Factor-alpha, Signal Transduction, Interleukin-6, Bone Marrow Transplantation, Mice, Knockout, Disease Progression, Inflammation Mediators, Interleukin-17, Collagen Type I, STAT3 Transcription Factor, Mice, Receptors, Interleukin-17, Interleukin-23, Transforming Growth Factor beta1, Hepatic Stellate Cells
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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