Dendritic Cell Regulation of Carbon Tetrachloride–Induced Murine Liver Fibrosis Regression
Open accessAbstract
Although hepatic fibrosis typically follows chronic inflammation, fibrosis will often regress after cessation of liver injury. In this study, we examined whether liver dendritic cells (DCs) play a role in liver fibrosis regression using carbon tetrachloride to induce liver injury. We examined DC dynamics during fibrosis regression and their capacity to modulate liver fibrosis regression upon cessation of injury. We show that conditional DC depletion soon after discontinuation of the liver insult leads to delayed fibrosis regression and reduced clearance of activated hepatic stellate cells, the key fibrogenic cell in the liver. Conversely, DC expansion induced either by Flt3L (fms–like tyrosine kinase–3 ligand) or adoptive transfer of purified DCs accelerates liver fibrosis regression. DC modulation of fibrosis was partially dependent on matrix metalloproteinase (MMP)–9, because MMP–9 inhibition abolished the Flt3L–mediated effect and the ability of transferred DCs to accelerate fibrosis regression. In contrast, transfer of DCs from MMP–9–deficient mice failed to improve fibrosis regression. Conclusion : Taken together, these results suggest that DCs increase fibrosis regression and that the effect is correlated with their production of MMP–9. The results also suggest that Flt3L treatment during fibrosis resolution merits evaluation to accelerate regression of advanced liver fibrosis. (Hepatology 2012;55:243–255)
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- Authors
- Jiao, J., Sastre, D., Fiel, M. I., Lee, U. E., Ghiassi–Nejad, Z., Ginhoux, F., Vivier, E., Friedman, S. L., Merad, M., & Aloman, C.
- Affiliations
- Icahn School of Medicine at Mount Sinai (US)
- Agency for Science, Technology and Research (SG)
- Corresponding author
- Aloman, Costica
- Venue
- Hepatology
- Published
- 2012-01
- Volume
- 55
- Issue
- 1
- Pages
- 244-255
- ISSN
- 0270-9139 (ISSN-L)
- PMC
- PMC3245345
- OpenAlex
- W1984834168
- Cited by
- 154
- References
- 55
- Citations by year
- 2026: 4 · 2025: 12 · 2024: 9 · 2023: 6 · 2022: 6 · 2021: 9 · 2020: 10 · 2019: 7 · 2018: 7 · 2017: 10 · 2016: 16 · 2015: 16 · 2014: 13 · 2013: 16 · 2012: 12
- FWCI
- 8.52
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Hepatology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- American Association for the Study of Liver Diseases
- National Institutes of Health (DK56621)
- National Institute on Alcohol Abuse and Alcoholism (K05AA018408)
- National Heart, Lung, and Blood Institute (HL086899, R01HL086899)
- National Cancer Institute (R01CA112100, CA112100, R01CA154947)
- National Institute of Diabetes and Digestive and Kidney Diseases (R56DK056621, R01DK056621, DK 56621)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Keywords
- liver fibrosis regression, dendritic cells, carbon tetrachloride-induced liver injury, hepatic stellate cells, Flt3L, MMP-9, dendritic cell depletion, fibrosis resolution
- MeSH terms
- Adjuvants, Immunologic, Animals, Carbon Tetrachloride Poisoning, Dendritic Cells, Female, Killer Cells, Natural, Liver Cirrhosis, Liver Regeneration, Membrane Proteins, Mice, Inbred C57BL, Mice, Transgenic, Phenotype, Adoptive Transfer, Matrix Metalloproteinase 9, Myeloid Cells, Mice, Chemical and Drug Induced Liver Injury
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