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Murine liver antigen presenting cells control suppressor activity of CD4+CD25+ regulatory T cells

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Murine liver antigen presenting cells control suppressor activity of CD4+CD25+ regulatory T cells. / Wiegard, Christiane; Frenzel, Christian; Herkel, Johannes; Kallen, Karl-Josef; Schmitt, Edgar; Lohse, Ansgar W.

In: HEPATOLOGY, Vol. 42, No. 1, 1, 07.2005, p. 193-199.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Wiegard, C, Frenzel, C, Herkel, J, Kallen, K-J, Schmitt, E & Lohse, AW 2005, 'Murine liver antigen presenting cells control suppressor activity of CD4+CD25+ regulatory T cells', HEPATOLOGY, vol. 42, no. 1, 1, pp. 193-199. https://doi.org/10.1002/hep.20756

APA

Wiegard, C., Frenzel, C., Herkel, J., Kallen, K-J., Schmitt, E., & Lohse, A. W. (2005). Murine liver antigen presenting cells control suppressor activity of CD4+CD25+ regulatory T cells. HEPATOLOGY, 42(1), 193-199. [1]. https://doi.org/10.1002/hep.20756

Vancouver

Wiegard C, Frenzel C, Herkel J, Kallen K-J, Schmitt E, Lohse AW. Murine liver antigen presenting cells control suppressor activity of CD4+CD25+ regulatory T cells. HEPATOLOGY. 2005 Jul;42(1):193-199. 1. https://doi.org/10.1002/hep.20756

Bibtex

@article{4fcf1fdd7c4b4f31bc23915e09ff0e32,
title = "Murine liver antigen presenting cells control suppressor activity of CD4+CD25+ regulatory T cells",
abstract = "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.",
keywords = "Animals, Antigen-Presenting Cells/physiology, CD4-Positive T-Lymphocytes/immunology, Cell Proliferation, Endothelial Cells/immunology, Hepatocytes/immunology, Immune Tolerance/immunology, Inflammation, Kupffer Cells/immunology, Liver/cytology, Mice, Receptors, Interleukin-2/immunology, T-Lymphocytes/immunology",
author = "Christiane Wiegard and Christian Frenzel and Johannes Herkel and Karl-Josef Kallen and Edgar Schmitt and Lohse, {Ansgar W}",
year = "2005",
month = jul,
doi = "10.1002/hep.20756",
language = "English",
volume = "42",
pages = "193--199",
journal = "HEPATOLOGY",
issn = "0270-9139",
publisher = "John Wiley and Sons Ltd",
number = "1",

}

RIS

TY - JOUR

T1 - Murine liver antigen presenting cells control suppressor activity of CD4+CD25+ regulatory T cells

AU - Wiegard, Christiane

AU - Frenzel, Christian

AU - Herkel, Johannes

AU - Kallen, Karl-Josef

AU - Schmitt, Edgar

AU - Lohse, Ansgar W

PY - 2005/7

Y1 - 2005/7

N2 - 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.

AB - 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.

KW - Animals

KW - Antigen-Presenting Cells/physiology

KW - CD4-Positive T-Lymphocytes/immunology

KW - Cell Proliferation

KW - Endothelial Cells/immunology

KW - Hepatocytes/immunology

KW - Immune Tolerance/immunology

KW - Inflammation

KW - Kupffer Cells/immunology

KW - Liver/cytology

KW - Mice

KW - Receptors, Interleukin-2/immunology

KW - T-Lymphocytes/immunology

U2 - 10.1002/hep.20756

DO - 10.1002/hep.20756

M3 - SCORING: Journal article

C2 - 15962311

VL - 42

SP - 193

EP - 199

JO - HEPATOLOGY

JF - HEPATOLOGY

SN - 0270-9139

IS - 1

M1 - 1

ER -