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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
Immunity (Cambridge, Mass.), 08/2013, Letnik: 39, Številka: 2Journal Article
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. Display omitted •IL-33 expression is upregulated in human and murine hepatic fibrosis•IL-33 release due to hepatocellular stress induces severe hepatic fibrosis in vivo•IL-33 expands liver resident innate lymphoid cells•IL-13 from ILC2 drives liver tissue remodeling by hepatic stellate cell activation
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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