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Inhibition of inflammatory CD4 T cell activity by murine liver sinusoidal endothelial cells

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Inhibition of inflammatory CD4 T cell activity by murine liver sinusoidal endothelial cells. / Carambia, Antonella; Frenzel, Christian; Bruns, Oliver T; Schwinge, Dorothee; Reimer, Rudolph; Hohenberg, Heinrich; Huber, Samuel; Tiegs, Gisa; Schramm, Christoph; Lohse, Ansgar W; Herkel, Johannes.

in: J HEPATOL, Jahrgang 58, Nr. 1, 01.01.2013, S. 112-8.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Carambia, A, Frenzel, C, Bruns, OT, Schwinge, D, Reimer, R, Hohenberg, H, Huber, S, Tiegs, G, Schramm, C, Lohse, AW & Herkel, J 2013, 'Inhibition of inflammatory CD4 T cell activity by murine liver sinusoidal endothelial cells', J HEPATOL, Jg. 58, Nr. 1, S. 112-8. https://doi.org/10.1016/j.jhep.2012.09.008

APA

Carambia, A., Frenzel, C., Bruns, O. T., Schwinge, D., Reimer, R., Hohenberg, H., Huber, S., Tiegs, G., Schramm, C., Lohse, A. W., & Herkel, J. (2013). Inhibition of inflammatory CD4 T cell activity by murine liver sinusoidal endothelial cells. J HEPATOL, 58(1), 112-8. https://doi.org/10.1016/j.jhep.2012.09.008

Vancouver

Carambia A, Frenzel C, Bruns OT, Schwinge D, Reimer R, Hohenberg H et al. Inhibition of inflammatory CD4 T cell activity by murine liver sinusoidal endothelial cells. J HEPATOL. 2013 Jan 1;58(1):112-8. https://doi.org/10.1016/j.jhep.2012.09.008

Bibtex

@article{e552a6ec052e4b5f89eef4a061327840,
title = "Inhibition of inflammatory CD4 T cell activity by murine liver sinusoidal endothelial cells",
abstract = "BACKGROUND & AIMS: The liver can mitigate the inflammatory activity of infiltrating T cells by mechanisms that are not entirely clear. Here we investigated the role of liver sinusoidal endothelial cells (LSECs) in regulating the activity of inflammatory CD4 T cells.METHODS: Interactions between T helper (Th) 1 or Th17 cells and LSEC were studied by intravital microscopy and by in vitro stimulation assays.RESULTS: Circulating CD4 T cells established lasting and repeated interactions with liver endothelium in vivo. Stimulation of Th1 and Th17 cells by LSEC greatly inhibited their capacity to secrete interferon-γ or interleukin-17 in vitro; in contrast, stimulation by dendritic cells (DCs) resulted in considerable secretion of both cytokines. Cytokine release by Th1 or Th17 cells seemed to be actively suppressed by LSEC, as indicated by the inhibition of cytokine secretion even in the presence of Th1- and Th17-promoting DC. This inhibition of CD4 T cell effector function seemed to depend on the dominance of inhibitory over activating co-stimulatory signals on LSEC, since (1) cytokine secretion could be restored by increased CD28 co-activation; (2) LSEC from interleukin-10(-/-) mice, which manifest increased activating signals, such as MHC II, and decreased inhibitory signals, such as PD-L1, failed to suppress cytokine secretion; and (3) cytokine secretion by Th1 or Th17 cells that lacked PD-1, the ligand for inhibitory PD-L1, could not be suppressed by LSEC.CONCLUSIONS: LSEC inhibit inflammatory cytokine secretion of Th1 and Th17 effector CD4 T cells in dependence of interleukin-10 and PD-1.",
keywords = "Animals, CD4-Positive T-Lymphocytes, Cell Communication, Cell Differentiation, Cells, Cultured, Dendritic Cells, Endothelial Cells, Female, Immune Tolerance, Interleukin-10, Liver, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Programmed Cell Death 1 Receptor, Signal Transduction, Th1 Cells, Th17 Cells",
author = "Antonella Carambia and Christian Frenzel and Bruns, {Oliver T} and Dorothee Schwinge and Rudolph Reimer and Heinrich Hohenberg and Samuel Huber and Gisa Tiegs and Christoph Schramm and Lohse, {Ansgar W} and Johannes Herkel",
note = "Copyright {\textcopyright} 2012 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.",
year = "2013",
month = jan,
day = "1",
doi = "10.1016/j.jhep.2012.09.008",
language = "English",
volume = "58",
pages = "112--8",
journal = "J HEPATOL",
issn = "0168-8278",
publisher = "Elsevier",
number = "1",

}

RIS

TY - JOUR

T1 - Inhibition of inflammatory CD4 T cell activity by murine liver sinusoidal endothelial cells

AU - Carambia, Antonella

AU - Frenzel, Christian

AU - Bruns, Oliver T

AU - Schwinge, Dorothee

AU - Reimer, Rudolph

AU - Hohenberg, Heinrich

AU - Huber, Samuel

AU - Tiegs, Gisa

AU - Schramm, Christoph

AU - Lohse, Ansgar W

AU - Herkel, Johannes

N1 - Copyright © 2012 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.

PY - 2013/1/1

Y1 - 2013/1/1

N2 - BACKGROUND & AIMS: The liver can mitigate the inflammatory activity of infiltrating T cells by mechanisms that are not entirely clear. Here we investigated the role of liver sinusoidal endothelial cells (LSECs) in regulating the activity of inflammatory CD4 T cells.METHODS: Interactions between T helper (Th) 1 or Th17 cells and LSEC were studied by intravital microscopy and by in vitro stimulation assays.RESULTS: Circulating CD4 T cells established lasting and repeated interactions with liver endothelium in vivo. Stimulation of Th1 and Th17 cells by LSEC greatly inhibited their capacity to secrete interferon-γ or interleukin-17 in vitro; in contrast, stimulation by dendritic cells (DCs) resulted in considerable secretion of both cytokines. Cytokine release by Th1 or Th17 cells seemed to be actively suppressed by LSEC, as indicated by the inhibition of cytokine secretion even in the presence of Th1- and Th17-promoting DC. This inhibition of CD4 T cell effector function seemed to depend on the dominance of inhibitory over activating co-stimulatory signals on LSEC, since (1) cytokine secretion could be restored by increased CD28 co-activation; (2) LSEC from interleukin-10(-/-) mice, which manifest increased activating signals, such as MHC II, and decreased inhibitory signals, such as PD-L1, failed to suppress cytokine secretion; and (3) cytokine secretion by Th1 or Th17 cells that lacked PD-1, the ligand for inhibitory PD-L1, could not be suppressed by LSEC.CONCLUSIONS: LSEC inhibit inflammatory cytokine secretion of Th1 and Th17 effector CD4 T cells in dependence of interleukin-10 and PD-1.

AB - BACKGROUND & AIMS: The liver can mitigate the inflammatory activity of infiltrating T cells by mechanisms that are not entirely clear. Here we investigated the role of liver sinusoidal endothelial cells (LSECs) in regulating the activity of inflammatory CD4 T cells.METHODS: Interactions between T helper (Th) 1 or Th17 cells and LSEC were studied by intravital microscopy and by in vitro stimulation assays.RESULTS: Circulating CD4 T cells established lasting and repeated interactions with liver endothelium in vivo. Stimulation of Th1 and Th17 cells by LSEC greatly inhibited their capacity to secrete interferon-γ or interleukin-17 in vitro; in contrast, stimulation by dendritic cells (DCs) resulted in considerable secretion of both cytokines. Cytokine release by Th1 or Th17 cells seemed to be actively suppressed by LSEC, as indicated by the inhibition of cytokine secretion even in the presence of Th1- and Th17-promoting DC. This inhibition of CD4 T cell effector function seemed to depend on the dominance of inhibitory over activating co-stimulatory signals on LSEC, since (1) cytokine secretion could be restored by increased CD28 co-activation; (2) LSEC from interleukin-10(-/-) mice, which manifest increased activating signals, such as MHC II, and decreased inhibitory signals, such as PD-L1, failed to suppress cytokine secretion; and (3) cytokine secretion by Th1 or Th17 cells that lacked PD-1, the ligand for inhibitory PD-L1, could not be suppressed by LSEC.CONCLUSIONS: LSEC inhibit inflammatory cytokine secretion of Th1 and Th17 effector CD4 T cells in dependence of interleukin-10 and PD-1.

KW - Animals

KW - CD4-Positive T-Lymphocytes

KW - Cell Communication

KW - Cell Differentiation

KW - Cells, Cultured

KW - Dendritic Cells

KW - Endothelial Cells

KW - Female

KW - Immune Tolerance

KW - Interleukin-10

KW - Liver

KW - Male

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Programmed Cell Death 1 Receptor

KW - Signal Transduction

KW - Th1 Cells

KW - Th17 Cells

U2 - 10.1016/j.jhep.2012.09.008

DO - 10.1016/j.jhep.2012.09.008

M3 - SCORING: Journal article

C2 - 22989568

VL - 58

SP - 112

EP - 118

JO - J HEPATOL

JF - J HEPATOL

SN - 0168-8278

IS - 1

ER -