Accumulation of natural killer T cells in progressive nonalcoholic fatty liver disease
Open accessAbstract
Liver inflammation is greater in nonalcoholic steatohepatitis (NASH) than steatosis, suggesting that immune responses contribute to nonalcoholic fatty liver disease (NAFLD) progression. Livers normally contain many natural killer T (NKT) cells that produce factors that modulate inflammatory and fibrogenic responses. Such cells are relatively depleted in steatosis, but their status in more advanced NAFLD is uncertain. We hypothesized that NKT cells accumulate and promote fibrosis progression in NASH. We aimed to determine if livers become enriched with NKT cells during NASH-related fibrosis; identify responsible mechanisms; and assess if NKT cells stimulate fibrogenesis. NKT cells were analyzed in wildtype mice and Patched-deficient (Ptc+/−) mice with an overly active Hedgehog (Hh) pathway, before and after feeding methionine choline-deficient (MCD) diets to induce NASH-related fibrosis. Effects of NKT cell-derived factors on hepatic stellate cells (HSC) were examined and fibrogenesis was evaluated in CD1d-deficient mice that lack NKT cells. NKT cells were quantified in human cirrhotic and nondiseased livers. During NASH-related fibrogenesis in wildtype mice, Hh pathway activation occurred, leading to induction of factors that promoted NKT cell recruitment, retention, and viability, plus liver enrichment with NKT cells. Ptc+/− mice accumulated more NKT cells and developed worse liver fibrosis; CD1d-deficient mice that lack NKT cells were protected from fibrosis. NKT cell-conditioned medium stimulated HSC to become myofibroblastic. Liver explants were 2-fold enriched with NKT cells in patients with non-NASH cirrhosis, and 4-fold enriched in patients with NASH cirrhosis. Conclusion : Hh pathway activation leads to hepatic enrichment with NKT cells that contribute to fibrosis progression in NASH. (Hepatology 2010;)
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Hepatic NKT cell numbers increase in human and mouse NASH.
“Hepatic NKT cell numbers increase in human and mouse NASH,92 and NASH and fibrosis are reduced in CD1d-deficient mice, which lack NKT cells.”
From Understanding the cellular interactome of non-alcoholic fatty liver disease (2022) · cites this paper as [92]
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- Authors
- Syn, W.-K., Oo, Y. H., Pereira, T. A., Karaca, G. F., Jung, Y., Omenetti, A., Witek, R. P., Choi, S. S., Guy, C. D., Fearing, C. M., Teaberry, V., Pereira, F. E. L., Adams, D. H., & Diehl, A. M.
- Affiliations
- Duke Medical Center (US)
- University of Birmingham (GB)
- Durham VA Health Care System (US)
- Corresponding author
- Diehl, Anna Mae
- ORCID
- Venue
- Hepatology
- Published
- 2010-06
- Volume
- 51
- Issue
- 6
- Pages
- 1998-2007
- ISSN
- 0270-9139 (ISSN-L)
- PMC
- PMC2920131
- OpenAlex
- W2040148868
- Cited by
- 283
- References
- 47
- Citations by year
- 2026: 5 · 2025: 11 · 2024: 10 · 2023: 25 · 2022: 25 · 2021: 15 · 2020: 25 · 2019: 14 · 2018: 19 · 2017: 15 · 2016: 24 · 2015: 15 · 2014: 14 · 2013: 21 · 2012: 20
- FWCI
- 15.36
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Hepatology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- University of Birmingham Research Portal (University of Birmingham) (submittedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK077794, R01DK053792)
- Topics
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Hepatology › Liver Diseases and Immunity
- Keywords
- NKT cells, nonalcoholic steatohepatitis, liver fibrosis, Hedgehog signaling, Patched1, hepatic stellate cells, myofibroblast differentiation, CD1d, liver cirrhosis, methionine-choline-deficient diet, liver inflammation
- MeSH terms
- Animals, Choline Deficiency, Fatty Liver, Fibrosis, Humans, Liver, Methionine, Mice, Inbred C57BL, Signal Transduction, Mice, Hedgehog Proteins, Hepatic Stellate Cells, Natural Killer T-Cells
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