ArticleFrontiers in immunology2026
Hepatitis C virus core protein-induced myeloid-derived suppressor cells promote hepatic fibrosis by regulating hepatic stellate cell function via TGF-β.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background and objective: Myeloid-derived suppressor cells (MDSCs) constitute a population of cells with immunosuppressive functions, potentially playing a pivotal role in the progression of chronic hepatitis C (CHC) to liver fibrosis. This study aimed to elucidate the molecular mechanisms by which HCVc-induced MDSCs interact with hepatic stellate cells to influence the onset and progression of liver fibrosis. Methods: CD14 Results: HCVc induced CD14 Conclusion: HCVc-induced MDSCs mediate the regulation of LX2 proliferation, activation, and apoptosis via TGF-β signaling, thereby promoting hepatic fibrosis. This "HCVc-MDSCs-TGF-β-LX2" axis establishes, for the first time, a direct link between viral infection, immunosuppressive myeloid cells, and the hepatic fibrosis process, providing potential targets for developing novel therapeutic strategies for hepatitis C-associated liver fibrosis.
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