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Hepatocytes induce Foxp3⁺ regulatory T cells by Notch signaling

Standard

Hepatocytes induce Foxp3⁺ regulatory T cells by Notch signaling. / Burghardt, Sven; Claass, Benjamin; Erhardt, Annette; Karimi, Khalil; Tiegs, Gisa.

in: J LEUKOCYTE BIOL, Jahrgang 96, Nr. 4, 01.10.2014, S. 571-7.

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

Harvard

Burghardt, S, Claass, B, Erhardt, A, Karimi, K & Tiegs, G 2014, 'Hepatocytes induce Foxp3⁺ regulatory T cells by Notch signaling', J LEUKOCYTE BIOL, Jg. 96, Nr. 4, S. 571-7. https://doi.org/10.1189/jlb.2AB0613-342RR

APA

Burghardt, S., Claass, B., Erhardt, A., Karimi, K., & Tiegs, G. (2014). Hepatocytes induce Foxp3⁺ regulatory T cells by Notch signaling. J LEUKOCYTE BIOL, 96(4), 571-7. https://doi.org/10.1189/jlb.2AB0613-342RR

Vancouver

Burghardt S, Claass B, Erhardt A, Karimi K, Tiegs G. Hepatocytes induce Foxp3⁺ regulatory T cells by Notch signaling. J LEUKOCYTE BIOL. 2014 Okt 1;96(4):571-7. https://doi.org/10.1189/jlb.2AB0613-342RR

Bibtex

@article{fd3c8df365ce4582a293d5b99dbbff3b,
title = "Hepatocytes induce Foxp3⁺ regulatory T cells by Notch signaling",
abstract = "The liver plays a pivotal role in maintaining immunological tolerance, although the exact molecular mechanism is still largely unknown. The induction of systemic tolerance by liver resident APCs has been attributed to peripheral deletion and to the induction of Tregs. HCs, the parenchymal cells in the liver, could function as nonprofessional APCs and interact and establish cell-cell contact with T lymphocytes. We hypothesized that HCs from healthy or regenerated livers may contribute to induction of functional Tregs. Here, we show that murine HCs induced Foxp3(+) Tregs within CD4(+) T cells in vitro, which increased in the presence of TGF-β. Interestingly, a further Foxp3(+) Treg expansion was observed if HCs were isolated from regenerated livers. Additionally, the induction of Foxp3(+) Tregs was associated with the Notch signaling pathway, as the ability of HCs to enhance Foxp3 was abolished by γ-secretase inhibition. Furthermore, HC-iTregs showed ability to suppress the proliferative response of CD4(+) T cells to anti-CD3 stimulation in vitro. Thus, HCs may play a pivotal role in the induction of tolerance via Notch-mediated conversion of CD4(+) T cells into Foxp3(+) Tregs upon TCR stimulation.",
keywords = "Animals, Calcium-Binding Proteins, Cytokines, Forkhead Transcription Factors, Hepatocytes, Intercellular Signaling Peptides and Proteins, Interleukin-2 Receptor alpha Subunit, Lymphocyte Activation, Lymphocyte Count, Male, Membrane Proteins, Mice, Models, Biological, Receptors, Notch, Signal Transduction, T-Lymphocyte Subsets, T-Lymphocytes, Regulatory, Transforming Growth Factor beta",
author = "Sven Burghardt and Benjamin Claass and Annette Erhardt and Khalil Karimi and Gisa Tiegs",
note = "{\textcopyright} 2014 Society for Leukocyte Biology.",
year = "2014",
month = oct,
day = "1",
doi = "10.1189/jlb.2AB0613-342RR",
language = "English",
volume = "96",
pages = "571--7",
journal = "J LEUKOCYTE BIOL",
issn = "0741-5400",
publisher = "FASEB",
number = "4",

}

RIS

TY - JOUR

T1 - Hepatocytes induce Foxp3⁺ regulatory T cells by Notch signaling

AU - Burghardt, Sven

AU - Claass, Benjamin

AU - Erhardt, Annette

AU - Karimi, Khalil

AU - Tiegs, Gisa

N1 - © 2014 Society for Leukocyte Biology.

PY - 2014/10/1

Y1 - 2014/10/1

N2 - The liver plays a pivotal role in maintaining immunological tolerance, although the exact molecular mechanism is still largely unknown. The induction of systemic tolerance by liver resident APCs has been attributed to peripheral deletion and to the induction of Tregs. HCs, the parenchymal cells in the liver, could function as nonprofessional APCs and interact and establish cell-cell contact with T lymphocytes. We hypothesized that HCs from healthy or regenerated livers may contribute to induction of functional Tregs. Here, we show that murine HCs induced Foxp3(+) Tregs within CD4(+) T cells in vitro, which increased in the presence of TGF-β. Interestingly, a further Foxp3(+) Treg expansion was observed if HCs were isolated from regenerated livers. Additionally, the induction of Foxp3(+) Tregs was associated with the Notch signaling pathway, as the ability of HCs to enhance Foxp3 was abolished by γ-secretase inhibition. Furthermore, HC-iTregs showed ability to suppress the proliferative response of CD4(+) T cells to anti-CD3 stimulation in vitro. Thus, HCs may play a pivotal role in the induction of tolerance via Notch-mediated conversion of CD4(+) T cells into Foxp3(+) Tregs upon TCR stimulation.

AB - The liver plays a pivotal role in maintaining immunological tolerance, although the exact molecular mechanism is still largely unknown. The induction of systemic tolerance by liver resident APCs has been attributed to peripheral deletion and to the induction of Tregs. HCs, the parenchymal cells in the liver, could function as nonprofessional APCs and interact and establish cell-cell contact with T lymphocytes. We hypothesized that HCs from healthy or regenerated livers may contribute to induction of functional Tregs. Here, we show that murine HCs induced Foxp3(+) Tregs within CD4(+) T cells in vitro, which increased in the presence of TGF-β. Interestingly, a further Foxp3(+) Treg expansion was observed if HCs were isolated from regenerated livers. Additionally, the induction of Foxp3(+) Tregs was associated with the Notch signaling pathway, as the ability of HCs to enhance Foxp3 was abolished by γ-secretase inhibition. Furthermore, HC-iTregs showed ability to suppress the proliferative response of CD4(+) T cells to anti-CD3 stimulation in vitro. Thus, HCs may play a pivotal role in the induction of tolerance via Notch-mediated conversion of CD4(+) T cells into Foxp3(+) Tregs upon TCR stimulation.

KW - Animals

KW - Calcium-Binding Proteins

KW - Cytokines

KW - Forkhead Transcription Factors

KW - Hepatocytes

KW - Intercellular Signaling Peptides and Proteins

KW - Interleukin-2 Receptor alpha Subunit

KW - Lymphocyte Activation

KW - Lymphocyte Count

KW - Male

KW - Membrane Proteins

KW - Mice

KW - Models, Biological

KW - Receptors, Notch

KW - Signal Transduction

KW - T-Lymphocyte Subsets

KW - T-Lymphocytes, Regulatory

KW - Transforming Growth Factor beta

U2 - 10.1189/jlb.2AB0613-342RR

DO - 10.1189/jlb.2AB0613-342RR

M3 - SCORING: Journal article

C2 - 24970859

VL - 96

SP - 571

EP - 577

JO - J LEUKOCYTE BIOL

JF - J LEUKOCYTE BIOL

SN - 0741-5400

IS - 4

ER -