Hepatic Stellate Cells Undermine the Allostimulatory Function of Liver Myeloid Dendritic Cells via STAT3-Dependent Induction of IDO
Open accessAbstract
Hepatic stellate cells (HSCs) are critical for hepatic wound repair and tissue remodeling. They also produce cytokines and chemokines that may contribute to the maintenance of hepatic immune homeostasis and the inherent tolerogenicity of the liver. The functional relationship between HSCs and the professional migratory APCs in the liver, that is, dendritic cells (DCs), has not been evaluated. In this article, we report that murine liver DCs colocalize with HSCs in vivo under normal, steady-state conditions, and cluster with HSCs in vitro. In vitro, HSCs secrete high levels of DC chemoattractants, such as MΙP-1α and MCP-1, as well as cytokines that modulate DC activation, including TNF-α, IL-6, and IL-1β. Culture of HSCs with conventional liver myeloid (m) DCs resulted in increased IL-6 and IL-10 secretion compared with that of either cell population alone. Coculture also resulted in enhanced expression of costimulatory (CD80, CD86) and coinhibitory (B7-H1) molecules on mDCs. HSC-induced mDC maturation required cell–cell contact and could be blocked, in part, by neutralizing MΙP-1α or MCP-1. HSC-induced mDC maturation was dependent on activation of STAT3 in mDCs and, in part, on HSC-secreted IL-6. Despite upregulation of costimulatory molecules, mDCs conditioned by HSCs demonstrated impaired ability to induce allogeneic T cell proliferation, which was independent of B7-H1, but dependent upon HSC-induced STAT3 activation and subsequent upregulation of IDO. In conclusion, by promoting IDO expression, HSCs may act as potent regulators of liver mDCs and function to maintain hepatic homeostasis and tolerogenicity.
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In co-culture experiments, HSCs interfere with T cell priming by dendritic cells via a CD54 (ICAM-1)-dependent signaling pathway and by inducing STAT3 signaling in DCs.
“In co-culture experiments, HSCs interfere with T cell priming by dendritic cells (DCs) via a CD54 (ICAM-1)-dependent signaling pathway and by inducing STAT3 signaling in DCs (44, 45).”
From Hepatic Stellate Cell-Immune Interactions in NASH (2022) · cites this paper as [44]
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Reply to: “Depletion of hepatic stellate cells: Have Kupffer cells lost their bad neighbor?”
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Research Progress on the Regulation of Tumor Microenvironment in Immunotherapy
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Liver Metastases from Colorectal Cancer: From Pathogenesis to Current Treatment
Fan, J.-L., Zhang, H.-R., Kong, D.-Y., Sun, Y., Lu, S.-B., Yang, W.-J., Xiang, R.-S., Zhang, Q., Pei, W., Zhang, H.-Z., et al. (2026) · MedComm · doi:10.1002/mco2.71044
- Authors
- Sumpter, T. L., Dangi, A., Matta, B. M., Huang, C., Stolz, D. B., Vodovotz, Y., Thomson, A. W., & Gandhi, C. R.
- Affiliations
- University of Pittsburgh (US)
- Department of Surgery, Thomas E. Starzl Transplantation Institute, University of Pittsburgh School of Medicine , Pittsburgh, PA 15213
- Corresponding author
- Dangi, Anil
- Huang, Chao
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2012-10
- Volume
- 189
- Issue
- 8
- Pages
- 3848-3858
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- PMC
- PMC3466356
- OpenAlex
- W1956469105
- Cited by
- 72
- References
- 90
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 3 · 2023: 4 · 2022: 5 · 2021: 6 · 2020: 6 · 2019: 7 · 2018: 6 · 2017: 7 · 2016: 3 · 2015: 5 · 2014: 6 · 2013: 6
- FWCI
- 3.44
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Veterans Affairs
- American Liver Foundation
- National Institutes of Health
- National Institute of General Medical Sciences (U54GM103529)
- National Institute of Allergy and Infectious Diseases (P01 AI81678, T32AI74490, P01AI081678, T32AI074490)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK054411)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Health Sciences › Medicine › Hepatology › Liver Diseases and Immunity
- Keywords
- hepatic stellate cells, dendritic cell maturation, STAT3 signaling, indoleamine 2,3-dioxygenase, allogeneic T cell proliferation, interleukin-6, chemokines, MIP-1α, MCP-1, costimulatory molecules, PD-L1, hepatic homeostasis
- MeSH terms
- Animals, Cells, Cultured, Dendritic Cells, Enzyme Induction, Isoantigens, Liver, Male, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Transgenic, Down-Regulation, Immunophenotyping, Mice, Knockout, Coculture Techniques, Myeloid Cells, Indoleamine-Pyrrole 2,3,-Dioxygenase, STAT3 Transcription Factor, Mice, Hepatic Stellate Cells
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