ArticleFrontiers in immunology2025
Extracellular vesicles of patients with acute-on-chronic liver failure induce mitochondrial dysfunction in T cells.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Reassessing the Prognostic Value of Circulating Extracellular Vesicles in Cirrhosis.Liver international : official journal of the International Association for the Study of the Liver · 2026Article
- Uncovering immune dysfunction in ACLF: Cellular mechanisms, molecular pathways, and therapeutic frontiers.Journal of hepatology · 2026Review
- Dihydroquercetin alleviates mitochondrial dysfunction and inhibits NLRP3-mediated pyroptosis in primary hepatocytes from chronic liver failure patients.American journal of translational research · 2026Article
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background and Aims: Liver cirrhosis and in particular acute-on-chronic liver failure (ACLF) are characterized by systemic inflammation and dysfunctional immune responses. Extracellular vesicles (EVs) are important mediators of cell stress and inflammation, but their role in ACLF is unclear. Methods: Phenotype and immune function of EVs of patients with compensated liver cirrhosis, acute decompensation, or ACLF were characterized regarding particle size, concentration, surface markers, and RNA cargo. In addition, functional analyses were performed to assess the impact of EVs on T cells. Results: EVs of patients with liver cirrhosis showed lower expression of exosome-specific markers (e.g. CD9, CD63, CD81) than EVs of healthy individuals, carried a distinct cargo of proteins and small RNAs, and were in high frequency derived from liver cells based on their carriage of liver cell markers such as ASGPR1, CD248 or CD163. Of note, in ACLF the concentration of EVs decreased, and EVs in ACLF lost partially their differentiation and surface markers but were enriched in lncRNAs. In functional assays, EVs of patients with cirrhosis and ACLF induced changes in the composition of T cell populations like a loss of naïve and central memory T cells and an increase in effector memory T cells. Mechanistically, EVs decreased the viability of CD3 Conclusion: Liver cirrhosis is associated with distinct changes in circulating EVs. In ACLF, EVs are less differentiated and induce mitochondrial dysfunction, decreased T cell viability and changes in the composition of T cell populations.
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