ArticleJournal of immunology (Baltimore, Md. : 1950)2011
Hepatic stellate cells function as regulatory bystanders.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
What it found
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Who cites it
77 citing papers in PubMed, 139 citations in OpenAlex.
- Pericytes in tissue fibrosis.American journal of physiology. Cell physiology · 2025Review
- Antifibrotic therapies for metabolic dysfunction-associated steatotic liver disease.JHEP reports : innovation in hepatology · 2025Review
- Hepatic stellate cells: balancing homeostasis, hepatoprotection and fibrogenesis in health and disease.Nature reviews. Gastroenterology & hepatology · 2025Review
- Role of PNPLA3 in Hepatic Stellate Cells and Hepatic Cellular Crosstalk.Liver international : official journal of the International Association for the Study of the Liver · 2025Review
- Vitamin A Metabolism and Resistance of Hepatic Metastases to Immunotherapy.Molecular cancer therapeutics · 2025Review
- The role of immune regulation in HBV infection and hepatocellular carcinogenesis.Frontiers in immunology · 2025Review
- Article
- Cellular uptake and in vivo distribution of mesenchymal-stem-cell-derived extracellular vesicles are protein corona dependent.Nature nanotechnology · 2024Article
- Role of the type 3 cytokines IL-17 and IL-22 in modulating metabolic dysfunction-associated steatotic liver disease.Frontiers in immunology · 2024Review
- Liver-Targeting Nanoplatforms for the Induction of Immune Tolerance.Nanomaterials (Basel, Switzerland) · 2023Review
- Analysis of the Role of Stellate Cell VCAM-1 in NASH Models in Mice.International journal of molecular sciences · 2023Article
- Interorgan communication with the liver: novel mechanisms and therapeutic targets.Frontiers in immunology · 2023Review
- Human Hepatic Stellate Cells: Isolation and Characterization.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Activated Hepatic Stellate Cells in Hepatocellular Carcinoma: Their Role as a Potential Target for Future Therapies.International journal of molecular sciences · 2022Review
- The immunological function of CXCR2 in the liver during sepsis.Journal of inflammation (London, England) · 2022Review
- Immunotherapy for hepatocellular carcinoma: A promising therapeutic option for advanced disease.World journal of hepatology · 2022Review
- An Eye on Kupffer Cells: Development, Phenotype and the Macrophage Niche.International journal of molecular sciences · 2022Review
- Tumor Microenvironment in Hepatocellular Carcinoma: Key Players for Immunotherapy.Journal of hepatocellular carcinoma · 2022Review
- Hepatic Stellate Cell-Immune Interactions in NASH.Frontiers in endocrinology · 2022Review
- Deciphering the Dynamic Complexities of the Liver Microenvironment - Toward a Better Understanding of Immune-Mediated liver Injury Caused by Immune Checkpoint Inhibitors (ILICI).The AAPS journal · 2021Review
17 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Regulatory T cells (Tregs) contribute significantly to the tolerogenic nature of the liver. The mechanisms, however, underlying liver-associated Treg induction are still elusive. We recently identified the vitamin A metabolite, retinoic acid (RA), as a key controller that promotes TGF-β-dependent Foxp3(+) Treg induction but inhibits TGF-β-driven Th17 differentiation. To investigate whether the RA producing hepatic stellate cells (HSC) are part of the liver tolerance mechanism, we investigated the ability of HSC to function as regulatory APC. Different from previous reports, we found that highly purified HSC did not express costimulatory molecules and only upregulated MHC class II after in vitro culture in the presence of exogenous IFN-γ. Consistent with an insufficient APC function, HSC failed to stimulate naive OT-II TCR transgenic CD4(+) T cells and only moderately stimulated α-galactosylceramide-primed invariant NKT cells. In contrast, HSC functioned as regulatory bystanders and promoted enhanced Foxp3 induction by OT-II TCR transgenic T cells primed by spleen dendritic cells, whereas they greatly inhibited the Th17 differentiation. Furthermore, the regulatory bystander capacity of the HSC was completely dependent on their ability to produce RA. Our data thus suggest that HSC can function as regulatory bystanders, and therefore, by promoting Tregs and suppressing Th17 differentiation, they might represent key players in the mechanism that drives liver-induced tolerance.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.