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Retinoic acid primes human dendritic cells to induce gut-homing, IL-10-producing regulatory T cells. / Bakdash, G.; Vogelpoel, L. T. C.; van Capel, T. M. M. et al.

In: Mucosal immunology, Vol. 8, No. 2, 2015, p. 265-278.

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Bakdash G, Vogelpoel LTC, van Capel TMM, Kapsenberg ML, de Jong EC. Retinoic acid primes human dendritic cells to induce gut-homing, IL-10-producing regulatory T cells. Mucosal immunology. 2015;8(2):265-278. doi: 10.1038/mi.2014.64

Author

Bakdash, G. ; Vogelpoel, L. T. C. ; van Capel, T. M. M. et al. / Retinoic acid primes human dendritic cells to induce gut-homing, IL-10-producing regulatory T cells. In: Mucosal immunology. 2015 ; Vol. 8, No. 2. pp. 265-278.

BibTeX

@article{bbd7ddac23fc47bbb6b8cb391d60a2d5,
title = "Retinoic acid primes human dendritic cells to induce gut-homing, IL-10-producing regulatory T cells",
abstract = "The vitamin A metabolite all-trans retinoic acid (RA) is an important determinant of intestinal immunity. RA primes dendritic cells (DCs) to express CD103 and produce RA themselves, which induces the gut-homing receptors α4β7 and CCR9 on T cells and amplifies transforming growth factor (TGF)-β-mediated development of Foxp3(+) regulatory T (Treg) cells. Here we investigated the effect of RA on human DCs and subsequent development of T cells. We report a novel role of RA in immune regulation by showing that RA-conditioned human DCs did not substantially enhance Foxp3 but induced α4β7(+) CCR9(+) T cells expressing high levels of interleukin (IL)-10, which were functional suppressive Treg cells. IL-10 production was dependent on DC-derived RA and was maintained when DCs were stimulated with toll-like receptor ligands. Furthermore, the presence of TGF-β during RA-DC-driven T-cell priming favored the induction of Foxp3(+) Treg cells over IL-10(+) Treg cells. Experiments with naive CD4(+) T cells stimulated by anti-CD3 and anti-CD28 antibodies in the absence of DCs emphasized that RA induces IL-10 in face of inflammatory mediators. The data thus show for the first time that RA induces IL-10-producing Treg cells and postulates a novel mechanism for IL-10 in maintaining tolerance to the intestinal microbiome",
author = "G. Bakdash and Vogelpoel, {L. T. C.} and {van Capel}, {T. M. M.} and Kapsenberg, {M. L.} and {de Jong}, {E. C.}",
year = "2015",
doi = "10.1038/mi.2014.64",
language = "English",
volume = "8",
pages = "265--278",
journal = "Mucosal immunology",
issn = "1933-0219",
publisher = "Nature Publishing Group",
number = "2",

}

RIS

TY - JOUR

T1 - Retinoic acid primes human dendritic cells to induce gut-homing, IL-10-producing regulatory T cells

AU - Bakdash, G.

AU - Vogelpoel, L. T. C.

AU - van Capel, T. M. M.

AU - Kapsenberg, M. L.

AU - de Jong, E. C.

PY - 2015

Y1 - 2015

N2 - The vitamin A metabolite all-trans retinoic acid (RA) is an important determinant of intestinal immunity. RA primes dendritic cells (DCs) to express CD103 and produce RA themselves, which induces the gut-homing receptors α4β7 and CCR9 on T cells and amplifies transforming growth factor (TGF)-β-mediated development of Foxp3(+) regulatory T (Treg) cells. Here we investigated the effect of RA on human DCs and subsequent development of T cells. We report a novel role of RA in immune regulation by showing that RA-conditioned human DCs did not substantially enhance Foxp3 but induced α4β7(+) CCR9(+) T cells expressing high levels of interleukin (IL)-10, which were functional suppressive Treg cells. IL-10 production was dependent on DC-derived RA and was maintained when DCs were stimulated with toll-like receptor ligands. Furthermore, the presence of TGF-β during RA-DC-driven T-cell priming favored the induction of Foxp3(+) Treg cells over IL-10(+) Treg cells. Experiments with naive CD4(+) T cells stimulated by anti-CD3 and anti-CD28 antibodies in the absence of DCs emphasized that RA induces IL-10 in face of inflammatory mediators. The data thus show for the first time that RA induces IL-10-producing Treg cells and postulates a novel mechanism for IL-10 in maintaining tolerance to the intestinal microbiome

AB - The vitamin A metabolite all-trans retinoic acid (RA) is an important determinant of intestinal immunity. RA primes dendritic cells (DCs) to express CD103 and produce RA themselves, which induces the gut-homing receptors α4β7 and CCR9 on T cells and amplifies transforming growth factor (TGF)-β-mediated development of Foxp3(+) regulatory T (Treg) cells. Here we investigated the effect of RA on human DCs and subsequent development of T cells. We report a novel role of RA in immune regulation by showing that RA-conditioned human DCs did not substantially enhance Foxp3 but induced α4β7(+) CCR9(+) T cells expressing high levels of interleukin (IL)-10, which were functional suppressive Treg cells. IL-10 production was dependent on DC-derived RA and was maintained when DCs were stimulated with toll-like receptor ligands. Furthermore, the presence of TGF-β during RA-DC-driven T-cell priming favored the induction of Foxp3(+) Treg cells over IL-10(+) Treg cells. Experiments with naive CD4(+) T cells stimulated by anti-CD3 and anti-CD28 antibodies in the absence of DCs emphasized that RA induces IL-10 in face of inflammatory mediators. The data thus show for the first time that RA induces IL-10-producing Treg cells and postulates a novel mechanism for IL-10 in maintaining tolerance to the intestinal microbiome

U2 - 10.1038/mi.2014.64

DO - 10.1038/mi.2014.64

M3 - Article

C2 - 25027601

VL - 8

SP - 265

EP - 278

JO - Mucosal immunology

JF - Mucosal immunology

SN - 1933-0219

IS - 2

ER -

ID: 2438018