Interleukin-17 signaling in inflammatory, Kupffer cells, and hepatic stellate cells exacerbates liver fibrosis in mice.

By Fanli Meng, Kai Wang, Tomonori Aoyama, S. Grivennikov, Y. Paik, D. Scholten, M. Cong, K. Iwaisako, Xiao Liu, Mingjun Zhang and 5 more. Gastroenterology, 2012

690 citations recorded by the source corpus.

Subfields: Epidemiology, Hepatology, Immunology

View Paper: https://www.semanticscholar.org/paper/c61690236921e3905b65c1652dbe3f3f07e32456

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

1. Robert F. Schwabe
2. E. Seki
3. Yukinori Koyama
4. D. Brenner
5. S. Friedman
6. F. Tacke

In Hepatology

1. E. Seki
2. D. Brenner
3. Robert F. Schwabe
4. Yukinori Koyama

In Immunology

1. D. Brenner
2. Robert F. Schwabe
3. E. Seki

Citations in the corpus

• Hepatic inflammatory responses in liver fibrosis (2023, neutral): “Although they can contribute to hepatic IL-17 production in mouse models of liver fibrosis 121,145 , which would suggest a profibrogenic function, they are also able to induce apoptosis of activated HSCs and increase natural killer cell-mediated cytotoxicity against activated HSCs, thereby limiting…”
• Liver inflammation and fibrosis. (2017, background): “Based on evidence from mouse models, IL-17 has a strong profibrogenic effect through two independent mechanisms (79).”
• Hepatic Inflammation and Fibrosis: Functional Links and Key Pathways (2015, background): “In experimental liver fibrosis, IL-17A stimulates both KCs and HSCs to produce IL-6, TNF-a, and TGF-b through activation of NF-jB and STAT3.(59,60) In addition to these proinflammatory activities, IL-17 also directly induces STAT3-dependent HSC activation.”
• Hepatic Stellate Cells and Liver Fibrosis (2013, neutral): “IL-17A may promote fibrosis by activating inflammatory and liver resident cells and inducing collagen type I production in HSCs through engagement of the signal transducer and activator of transcription 3 signaling pathway (181).”