Murine Liver Antigen Presenting Cells Control Suppressor Activity of CD4+CD25+ Regulatory T Cells *
Open accessAbstract
CD4+CD25+ regulatory T cells (Treg) are important mediators of peripheral immune tolerance; however, whether Treg participate also in hepatic immune tolerance is not clear. Therefore, we tested the potential of Treg to suppress stimulation of CD4+ T cells by liver sinusoidal endothelial cells (LSEC), Kupffer cells (KC), or hepatocytes. In the absence of Treg, all 3 types of liver cells could stimulate CD4+ T cell proliferation; in the presence of Treg, however, CD4+ T cell proliferation was suppressed. Interaction with KC even stimulated the expansion of the Treg population; LSEC or hepatocytes, in contrast, could not induce proliferation of Treg. Because liver inflammation can be induced by infection, we tested the potential of liver cells to modify Treg suppressor activity in the presence of microbial signals. In the presence of immune-stimulatory CpG-oligonucleotides, LSEC, KC, and hepatocytes could indeed overcome Treg-mediated suppression; in the presence of lipopolysaccharide (LPS), however, only KC and hepatocytes, but not LSEC, could overcome Treg suppressor activity. Hepatocytes from mice with deficient toll-like receptor-4 signaling failed to abrogate Treg suppression in response to LPS, indicating that overcoming Treg suppressor activity was indeed a response of the liver cell and not of the Treg. In conclusion , Treg can suppress CD4+ T cell stimulation by liver cells. However, in response to microbial signals, the liver cells can overcome the suppressive activity of Treg. Thus, liver cells may facilitate the transition from hepatic immune tolerance to hepatic inflammation by controlling Treg suppressor activity. (Hepatology 2005;42:193–199.)
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MHC class II antigen presentation by hepatocytes cannot trigger effective activation of T cells, and in turn might favour a chronic viral infection over viral clearance.
“This evidence suggests that the fate of MHC class II antigen presentation by the hepatocyte cannot trigger an effective activation of the T cells, and in turn it might favour a chronic viral infection over viral clearance(31, 39-41).”
From The liver as a central "hub" of the immune system: pathophysiological implications (2025) · cites this paper as [31]
The Discussion (page not available) reports that hepatocytes can induce regulatory T-cell suppression, which supports the possibility of reduced T-cell responses. But the Abstract reports that hepatocytes stimulated CD4+ T-cell proliferation without regulatory T cells, and the Discussion says they can overcome suppression in response to microbial signals. The paper does not establish that hepatocyte antigen presentation cannot produce effective activation or that it favours chronic viral infection over clearance. (LLM, conf=0.82)
Experimental — accuracy not yet measuredA liver-resident population of auto-aggressive CD8+ T cells is responsible for MHC class I-independent killing of liver cells in direct response to metabolic stimuli.
“Similarly, it has recently been shown that a liver-resident population of 'auto-aggressive' CD8+ T cells is responsible for MHC class I-independent killing of liver cells in direct response to metabolic stimuli (31) .”
From The liver as a central "hub" of the immune system: pathophysiological implications (2025) · cites this paper as [31]
The Discussion (page not available in our copy) mentions CD8+ T-cell-mediated autoimmunity against hepatocytes after CpG-ODN administration. It does not describe a liver-resident CD8+ population, MHC class I-independent killing, or a direct response to metabolic stimuli; instead, it discusses microbial signals acting through liver antigen-presenting cells. (LLM, conf=0.86)
Experimental — accuracy not yet measuredConstitutive expression of MHC class II on hepatocytes in murine models of choriomeningitis virus infection increases the duration of the infection and reduces production of pro-inflammatory cytokines (IFN-γ) by virus-specific CD4+ and CD8+ T cells.
“Constitutive expression of MHC class II on hepatocytes in murine models of choriomeningitis virus infection has shown to increase the duration of the infection, reducing the production of pro-inflammatory cytokines (i.e. IFN-γ) by virus-specific CD4 + T and CD8 + T cells.”
From The liver as a central "hub" of the immune system: pathophysiological implications (2025) · cites this paper as [31]
The Discussion (page unavailable) says hepatocytes can upregulate MHC class II during liver inflammation; it identifies Kupffer cells and liver sinusoidal endothelial cells as constitutively expressing it. Neither that passage nor the other passages found in our copy reports a murine choriomeningitis virus experiment, infection duration, or IFN-γ production by virus-specific CD4+ and CD8+ T cells. Searches for those outcomes did not locate supporting evidence. (LLM, conf=0.76)
Experimental — accuracy not yet measured
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- Authors
- Wiegard, C., Frenzel, C., Herkel, J., Kallen, K.-J., Schmitt, E., & Lohse, A. W.
- Affiliations
- University Medical Center Hamburg-Eppendorf (DE)
- Johannes Gutenberg University Mainz (DE)
- Christian-Albrechts-Universität zu Kiel (DE)
- Corresponding author
- Herkel, Johannes
- Venue
- Hepatology
- Published
- 2005-07
- Volume
- 42
- Issue
- 1
- Pages
- 193-199
- ISSN
- 0270-9139 (ISSN-L)
- OpenAlex
- W1998525935
- Cited by
- 97
- References
- 21
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 2 · 2023: 1 · 2022: 2 · 2021: 2 · 2020: 3 · 2019: 1 · 2018: 8 · 2017: 5 · 2016: 7 · 2015: 8 · 2014: 4 · 2013: 5 · 2012: 7
- FWCI
- 2.60
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Hepatology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Deutsche Forschungsgemeinschaft (SFB 490)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Hepatology › Liver Diseases and Immunity
- Keywords
- regulatory T cells, CD4+CD25+ T cells, Kupffer cells, liver sinusoidal endothelial cells, hepatocytes, T cell suppression, liver inflammation, TLR4, lipopolysaccharide, CpG oligodeoxynucleotides, microbial signals
- MeSH terms
- Animals, Antigen-Presenting Cells, Immune Tolerance, Inflammation, Kupffer Cells, Liver, T-Lymphocytes, Receptors, Interleukin-2, CD4-Positive T-Lymphocytes, Hepatocytes, Endothelial Cells, Cell Proliferation, Mice
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