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Connecting liver and gut: murine liver sinusoidal endothelium induces gut tropism of CD4+ T cells via retinoic acid

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Connecting liver and gut: murine liver sinusoidal endothelium induces gut tropism of CD4+ T cells via retinoic acid. / Neumann, Katrin; Kruse, Nils; Szilagyi, Balint; Erben, Ulrike; Rudolph, Christine; Flach, Anne; Zeitz, Martin; Hamann, Alf; Klugewitz, Katja.

in: HEPATOLOGY, Jahrgang 55, Nr. 6, 06.2012, S. 1976-84.

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

Harvard

Neumann, K, Kruse, N, Szilagyi, B, Erben, U, Rudolph, C, Flach, A, Zeitz, M, Hamann, A & Klugewitz, K 2012, 'Connecting liver and gut: murine liver sinusoidal endothelium induces gut tropism of CD4+ T cells via retinoic acid', HEPATOLOGY, Jg. 55, Nr. 6, S. 1976-84. https://doi.org/10.1002/hep.24816

APA

Neumann, K., Kruse, N., Szilagyi, B., Erben, U., Rudolph, C., Flach, A., Zeitz, M., Hamann, A., & Klugewitz, K. (2012). Connecting liver and gut: murine liver sinusoidal endothelium induces gut tropism of CD4+ T cells via retinoic acid. HEPATOLOGY, 55(6), 1976-84. https://doi.org/10.1002/hep.24816

Vancouver

Neumann K, Kruse N, Szilagyi B, Erben U, Rudolph C, Flach A et al. Connecting liver and gut: murine liver sinusoidal endothelium induces gut tropism of CD4+ T cells via retinoic acid. HEPATOLOGY. 2012 Jun;55(6):1976-84. https://doi.org/10.1002/hep.24816

Bibtex

@article{64ccdc273cf64cf7a2858aa5dc0e52ac,
title = "Connecting liver and gut: murine liver sinusoidal endothelium induces gut tropism of CD4+ T cells via retinoic acid",
abstract = "UNLABELLED: Gut-activated T cells migrating into the liver can cause extraintestinal manifestations of inflammatory bowel disease. T cells acquire a gut-homing phenotype dependent on retinoic acid (RA) provided by intestinal dendritic cells (DC). We investigated whether liver antigen-presenting cells can induce gut tropism supporting an enterohepatic lymphocyte circulation. Priming of CD4(+) T cells by liver sinusoidal endothelial cells (LSEC) supported migration into gut and gut-associated lymphoid tissue. As observed for T cells primed by intestinal DCs, this gut tropism depended on α(4) β(7) integrin and CC chemokine receptor 9 (CCR9) expression by LSEC-primed CD4(+) T cells. The induction of gut-homing molecules was mediated by RA, a derivate of vitamin A that is stored in large amounts within the liver. LSECs expressed functional retinal dehydrogenases and could convert vitamin A to RA. Conversely, the lack of signaling via the RA receptor prevented the expression of α(4) β(7) integrin and CCR9 on LSEC-primed CD4(+) T cells, consequently reducing their in vivo migration to the intestine. Other liver antigen-presenting cells failed to support high expression of α(4) β(7) integrin on CD4(+) T cells, thus, the potential to induce gut homing is restricted to LSECs.CONCLUSION: The capacity to promote gut tropism via vitamin A use is not unique for intestinal DCs but is also a feature of LSECs. Our data support the assumption that CD4(+) T cells can migrate from the liver to the gut as one branch of a postulated enterohepatic lymphocyte circulation.",
keywords = "Aldehyde Oxidoreductases, Amino Acid Sequence, Animals, CD4-Positive T-Lymphocytes, Cell Movement, Endothelial Cells, Enterohepatic Circulation, Integrins, Intestines, Isoenzymes, Liver, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Molecular Sequence Data, Receptors, CCR, Retinal Dehydrogenase, Tretinoin, Tropism",
author = "Katrin Neumann and Nils Kruse and Balint Szilagyi and Ulrike Erben and Christine Rudolph and Anne Flach and Martin Zeitz and Alf Hamann and Katja Klugewitz",
note = "Copyright {\textcopyright} 2011 American Association for the Study of Liver Diseases.",
year = "2012",
month = jun,
doi = "10.1002/hep.24816",
language = "English",
volume = "55",
pages = "1976--84",
journal = "HEPATOLOGY",
issn = "0270-9139",
publisher = "John Wiley and Sons Ltd",
number = "6",

}

RIS

TY - JOUR

T1 - Connecting liver and gut: murine liver sinusoidal endothelium induces gut tropism of CD4+ T cells via retinoic acid

AU - Neumann, Katrin

AU - Kruse, Nils

AU - Szilagyi, Balint

AU - Erben, Ulrike

AU - Rudolph, Christine

AU - Flach, Anne

AU - Zeitz, Martin

AU - Hamann, Alf

AU - Klugewitz, Katja

N1 - Copyright © 2011 American Association for the Study of Liver Diseases.

PY - 2012/6

Y1 - 2012/6

N2 - UNLABELLED: Gut-activated T cells migrating into the liver can cause extraintestinal manifestations of inflammatory bowel disease. T cells acquire a gut-homing phenotype dependent on retinoic acid (RA) provided by intestinal dendritic cells (DC). We investigated whether liver antigen-presenting cells can induce gut tropism supporting an enterohepatic lymphocyte circulation. Priming of CD4(+) T cells by liver sinusoidal endothelial cells (LSEC) supported migration into gut and gut-associated lymphoid tissue. As observed for T cells primed by intestinal DCs, this gut tropism depended on α(4) β(7) integrin and CC chemokine receptor 9 (CCR9) expression by LSEC-primed CD4(+) T cells. The induction of gut-homing molecules was mediated by RA, a derivate of vitamin A that is stored in large amounts within the liver. LSECs expressed functional retinal dehydrogenases and could convert vitamin A to RA. Conversely, the lack of signaling via the RA receptor prevented the expression of α(4) β(7) integrin and CCR9 on LSEC-primed CD4(+) T cells, consequently reducing their in vivo migration to the intestine. Other liver antigen-presenting cells failed to support high expression of α(4) β(7) integrin on CD4(+) T cells, thus, the potential to induce gut homing is restricted to LSECs.CONCLUSION: The capacity to promote gut tropism via vitamin A use is not unique for intestinal DCs but is also a feature of LSECs. Our data support the assumption that CD4(+) T cells can migrate from the liver to the gut as one branch of a postulated enterohepatic lymphocyte circulation.

AB - UNLABELLED: Gut-activated T cells migrating into the liver can cause extraintestinal manifestations of inflammatory bowel disease. T cells acquire a gut-homing phenotype dependent on retinoic acid (RA) provided by intestinal dendritic cells (DC). We investigated whether liver antigen-presenting cells can induce gut tropism supporting an enterohepatic lymphocyte circulation. Priming of CD4(+) T cells by liver sinusoidal endothelial cells (LSEC) supported migration into gut and gut-associated lymphoid tissue. As observed for T cells primed by intestinal DCs, this gut tropism depended on α(4) β(7) integrin and CC chemokine receptor 9 (CCR9) expression by LSEC-primed CD4(+) T cells. The induction of gut-homing molecules was mediated by RA, a derivate of vitamin A that is stored in large amounts within the liver. LSECs expressed functional retinal dehydrogenases and could convert vitamin A to RA. Conversely, the lack of signaling via the RA receptor prevented the expression of α(4) β(7) integrin and CCR9 on LSEC-primed CD4(+) T cells, consequently reducing their in vivo migration to the intestine. Other liver antigen-presenting cells failed to support high expression of α(4) β(7) integrin on CD4(+) T cells, thus, the potential to induce gut homing is restricted to LSECs.CONCLUSION: The capacity to promote gut tropism via vitamin A use is not unique for intestinal DCs but is also a feature of LSECs. Our data support the assumption that CD4(+) T cells can migrate from the liver to the gut as one branch of a postulated enterohepatic lymphocyte circulation.

KW - Aldehyde Oxidoreductases

KW - Amino Acid Sequence

KW - Animals

KW - CD4-Positive T-Lymphocytes

KW - Cell Movement

KW - Endothelial Cells

KW - Enterohepatic Circulation

KW - Integrins

KW - Intestines

KW - Isoenzymes

KW - Liver

KW - Mice

KW - Mice, Inbred BALB C

KW - Mice, Inbred C57BL

KW - Molecular Sequence Data

KW - Receptors, CCR

KW - Retinal Dehydrogenase

KW - Tretinoin

KW - Tropism

U2 - 10.1002/hep.24816

DO - 10.1002/hep.24816

M3 - SCORING: Journal article

C2 - 22109893

VL - 55

SP - 1976

EP - 1984

JO - HEPATOLOGY

JF - HEPATOLOGY

SN - 0270-9139

IS - 6

ER -