Natural killer cells ameliorate liver fibrosis by killing activated stellate cells in NKG2D-dependent and tumor necrosis factor-related apoptosis-inducing ligand-dependent manners.

By S. Radaeva, R. Sun, B. Jaruga, V. Nguyen, Zhigang Tian, B. Gao. Gastroenterology, 2006

597 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/dff820e81bc7f29f1b4e90e525a48eb279a86d08

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In Hepatology

In Immunology

Citations in the corpus

Hepatic stellate cells as key target in liver fibrosis (2017, background): “Natural killer (NK) cells kill senescentHSCs and produce interferonγ (IFNγ) that induces apoptosis and cell cycle arrest in HSCs [76].”
Liver Fibrosis: Mechanistic Concepts and Therapeutic Perspectives (2020, background): “Innate cytokines [207], natural killer (NK) cells [208], and macrophages [209] have been reported to inhibit liver fibrosis by clearance or inactivation of HSCs and therefore may underlie decompensation of the physiological balance of pro- and anti-fibrogenic mechanisms in chronic ASH.”
Recent advances in 2D and 3D in vitro systems using primary hepatocytes, alternative hepatocyte sources and non-parenchymal liver cells and their use in investigating mechanisms of hepatotoxicity, cell signaling and ADME (2013, unknown): “Their role in pathology is mostly addressed in conditions of chronic liver damage, where their main function is the deposition of ECM, which limits the progression of injury and favors tissue regeneration (Bataller and Brenner 2005; Radaeva et al. 2006).”
Hepatic Stellate Cells and Liver Fibrosis (2013, unknown): “Hepatocytes can secrete NGF, which is apoptotic towards stellate cells (228) (203).”
Senescence of activated stellate cells limits liver fibrosis (2008, methodology): “To deplete NK cells we treated mice with neutralizing antibodies (anti-AsialoGM1 [Radaeva et al., 2006; Xue et al., 2007]) during the period following CCl4 withdrawal.”
Regulation of ligands for the NKG2D activating receptor (2013, background): “Indeed, induced expression of NKG2D ligands may enable NK cells to eliminate senescent cells and thereby aid in resolving the injury (56, 58).”
Hepatic inflammatory responses in liver fibrosis (2023, unknown): “Specifically, hepatic γδ T cells, as well as tissue-resident memory CD8 + T cells, induce HSC apoptosis via the FAS–FAS-ligand pathway 61,135 , whereas natural killer cells kill HSCs via NKG2D and tumour necrosis factor-related apoptosis-inducing ligand-mediated pathways 204 .”
Hepatic Inflammation and Fibrosis: Functional Links and Key Pathways (2015, background): “Accordingly, treatment with type I or II IFNs suppresses experimental liver fibrosis.(7,77,78) In addition to direct antifibrogenic effects on HSCs, IFN-c also promotes activation of NK cells that, in turn, kill activated HSCs, thereby ameliorating liver fibrosis.”