Interleukin-17A plays a pivotal role in cholestatic liver fibrosis in mice

Hara, Michio; Kono, Hiroshi; Furuya, Shinichi; Hirayama, Kazuyoshi; Tsuchiya, Mai; Fujii, Hideki

doi:10.1016/j.jss.2013.03.025

Cited by 36 publications

(28 citation statements)

References 32 publications

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“…31 In rodents, IL-17A deficiency protects from CCl 4 and bile duct ligation induced liver fibrosis. [31][32][33] Therefore, IL-17 neutralization may be a promising approach for anti-fibrotic therapy in patients with chronic liver diseases. In the mouse model however, animals die before developing pronounced fibrosis, thus the effect of IL-17 neutralization on fibrosis cannot be assessed in the rodent model 4 .…”

Section: Accepted Manuscriptmentioning

confidence: 99%

Interleukin 17, Produced by γδ T Cells, Contributes to Hepatic Inflammation in a Mouse Model of Biliary Atresia and Is Increased in Livers of Patients

et al. 2016

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Section: Accepted Manuscriptmentioning

confidence: 99%

Interleukin 17, Produced by γδ T Cells, Contributes to Hepatic Inflammation in a Mouse Model of Biliary Atresia and Is Increased in Livers of Patients

et al. 2016

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“…Intriguingly, liver resident cells such as Kupffer cells and hepatic stellate cells (HSC) can also show strong expression of IL-17 cytokines and their receptors in addition to Th17. Furthermore, IL-17 could stimulate the production of TNF- α and TGF- β from Kupffer cells, which then regulate the HSC activation via the Stat-3 signaling pathway and in turn promote the differentiation of IL-17 expressing cells [68, 69]. To date, however, there is no ideal single animal model that can demonstrate that all the characteristic of PSC patients exists.…”

Section: Pathological Roles Of Il-17 In Autoimmune Liver Diseasesmentioning

confidence: 99%

Therapeutic Potential of IL‐17‐Mediated Signaling Pathway in Autoimmune Liver Diseases

Zhang

Bernuzzi

Lleo

et al. 2015

Mediators of Inflammation

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Emerging evidence reveals that various cytokines and tissue microenvironments contribute to liver inflammation and autoimmunity, and IL-17 family is one of highlights acknowledged. Although the implication of IL-17 family in most common autoimmune diseases (such as psoriasis, inflammatory bowel disease, and rheumatoid arthritis) has been extensively characterized, the role of this critical family in pathophysiology of autoimmune liver diseases (AILD) still needs to be clarified. In the review, we look into the intriguing biology of IL-17 family and further dissect on the intricate role of IL-17-mediated pathway in AILD. Considering encouraging data from preclinical and clinical trials, IL-17 targeted therapy has shown promises in several certain autoimmune conditions. However, blocking IL-17-mediated pathway is just beginning, and more fully investigation and reflection are required. Taking together, targeting IL-17-mediated responses may open up new areas of potential clinical treatment for AILD.

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“…A study using IL-17A knockout mice has shown that IL-17A deficiency attenuates BDL-induced liver damage and expression levels of TNF-a and transforming growth factor-b. 40 This study has also shown that Kupffer cells treated with IL-17A secrete significantly higher levels of TNF-a and transforming growth factor-b induced by LPS. Another study has shown that neutralization of IL-17A by antieIL-17A antibody attenuates BDL-induced fibrosis and proinflammatory cytokine expression, including TNF-a and IL-6.…”

Section: Activation Of Kupffer Cellsmentioning

confidence: 58%