ArticleJHEP reports : innovation in hepatology2026
Mycobiome dysbiosis and genetic predisposition to elevated IL-17A contribute to fibrosis in MASLD.
Article in JHEP reports : innovation in hepatology, 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 & Aims: Metabolic dysfunction-associated steatotic liver disease (MASLD) is the leading cause of chronic liver disease in Western countries. Progression to metabolic dysfunction-associated steatohepatitis (MASH) occurs when fat accumulation in the liver triggers inflammatory processes including T helper 17 cell (Th17) activation. We aimed to investigate the role of intestinal fungi in MASH-mediating Th17-associated signaling. Methods: Blood samples from patients with MASLD (n = 451), including 141 with histology-proven MASH, were genotyped for Results: We identified the Conclusions: Genetic predisposition to enhanced Th17 responses, in the context of mycobiome dysbiosis, may promote MASH progression and liver fibrosis. Impact and implications: Liver inflammation and fibrosis are key drivers of the transition from bland steatosis to metabolic dysfunction-associated steatohepatitis (MASH). Our findings identify a combinatorial mechanism in which genetic predisposition to enhanced IL-17A signaling, together with gut mycobiome dysbiosis, promotes MASH development and fibrosis progression. This work highlights the importance of host-mycobiome interactions in shaping inflammatory liver disease and supports further investigation into targeted strategies aimed at modulating IL-17A-mediated immune responses in patients with MASLD. Such approaches may offer novel opportunities for risk stratification and therapeutic intervention.
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