Oxysterol Sensing through the Receptor GPR183 Promotes the Lymphoid-Tissue-Inducing Function of Innate Lymphoid Cells and Colonic Inflammation

Standard

Oxysterol Sensing through the Receptor GPR183 Promotes the Lymphoid-Tissue-Inducing Function of Innate Lymphoid Cells and Colonic Inflammation. / Emgård, Johanna; Kammoun, Hana; García-Cassani, Bethania; Chesné, Julie; Parigi, Sara M; Jacob, Jean-Marie; Cheng, Hung-Wei; Evren, Elza; Das, Srustidhar; Czarnewski, Paulo; Sleiers, Natalie; Melo-Gonzalez, Felipe; Kvedaraite, Egle; Svensson, Mattias; Scandella, Elke; Hepworth, Matthew R; Huber, Samuel; Ludewig, Burkhard; Peduto, Lucie; Villablanca, Eduardo J; Veiga-Fernandes, Henrique; Pereira, João P; Flavell, Richard A; Willinger, Tim.

in: IMMUNITY, Jahrgang 48, Nr. 1, 16.01.2018, S. 120-132.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

Emgård, J, Kammoun, H, García-Cassani, B, Chesné, J, Parigi, SM, Jacob, J-M, Cheng, H-W, Evren, E, Das, S, Czarnewski, P, Sleiers, N, Melo-Gonzalez, F, Kvedaraite, E, Svensson, M, Scandella, E, Hepworth, MR, Huber, S, Ludewig, B, Peduto, L, Villablanca, EJ, Veiga-Fernandes, H, Pereira, JP, Flavell, RA & Willinger, T 2018, 'Oxysterol Sensing through the Receptor GPR183 Promotes the Lymphoid-Tissue-Inducing Function of Innate Lymphoid Cells and Colonic Inflammation', IMMUNITY, Jg. 48, Nr. 1, S. 120-132. https://doi.org/10.1016/j.immuni.2017.11.020

APA

Emgård, J., Kammoun, H., García-Cassani, B., Chesné, J., Parigi, S. M., Jacob, J-M., Cheng, H-W., Evren, E., Das, S., Czarnewski, P., Sleiers, N., Melo-Gonzalez, F., Kvedaraite, E., Svensson, M., Scandella, E., Hepworth, M. R., Huber, S., Ludewig, B., Peduto, L., ... Willinger, T. (2018). Oxysterol Sensing through the Receptor GPR183 Promotes the Lymphoid-Tissue-Inducing Function of Innate Lymphoid Cells and Colonic Inflammation. IMMUNITY, 48(1), 120-132. https://doi.org/10.1016/j.immuni.2017.11.020

Vancouver

Bibtex

@article{039686fc2d574b72a63a5f3fdb4fac3c,
title = "Oxysterol Sensing through the Receptor GPR183 Promotes the Lymphoid-Tissue-Inducing Function of Innate Lymphoid Cells and Colonic Inflammation",
abstract = "Group 3 innate lymphoid cells (ILC3s) sense environmental signals and are critical for tissue integrity in the intestine. Yet, which signals are sensed and what receptors control ILC3 function remain poorly understood. Here, we show that ILC3s with a lymphoid-tissue-inducer (LTi) phenotype expressed G-protein-coupled receptor 183 (GPR183) and migrated to its oxysterol ligand 7α,25-hydroxycholesterol (7α,25-OHC). In mice lacking Gpr183 or 7α,25-OHC, ILC3s failed to localize to cryptopatches (CPs) and isolated lymphoid follicles (ILFs). Gpr183 deficiency in ILC3s caused a defect in CP and ILF formation in the colon, but not in the small intestine. Localized oxysterol production by fibroblastic stromal cells provided an essential signal for colonic lymphoid tissue development, and inflammation-induced increased oxysterol production caused colitis through GPR183-mediated cell recruitment. Our findings show that GPR183 promotes lymphoid organ development and indicate that oxysterol-GPR183-dependent positioning within tissues controls ILC3 activity and intestinal homeostasis.",
keywords = "Animals, Cell Movement, Colitis, Colon, Cytokines, Flow Cytometry, Fluorescent Antibody Technique, Ligands, Lymphocytes, Lymphoid Tissue, Mice, Oxysterols, Real-Time Polymerase Chain Reaction, Receptors, G-Protein-Coupled, Signal Transduction, Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't",
author = "Johanna Emg{\aa}rd and Hana Kammoun and Bethania Garc{\'i}a-Cassani and Julie Chesn{\'e} and Parigi, {Sara M} and Jean-Marie Jacob and Hung-Wei Cheng and Elza Evren and Srustidhar Das and Paulo Czarnewski and Natalie Sleiers and Felipe Melo-Gonzalez and Egle Kvedaraite and Mattias Svensson and Elke Scandella and Hepworth, {Matthew R} and Samuel Huber and Burkhard Ludewig and Lucie Peduto and Villablanca, {Eduardo J} and Henrique Veiga-Fernandes and Pereira, {Jo{\~a}o P} and Flavell, {Richard A} and Tim Willinger",
note = "Copyright {\textcopyright} 2017 The Authors. Published by Elsevier Inc. All rights reserved.",
year = "2018",
month = jan,
day = "16",
doi = "10.1016/j.immuni.2017.11.020",
language = "English",
volume = "48",
pages = "120--132",
journal = "IMMUNITY",
issn = "1074-7613",
publisher = "Cell Press",
number = "1",

}

RIS

TY - JOUR

T1 - Oxysterol Sensing through the Receptor GPR183 Promotes the Lymphoid-Tissue-Inducing Function of Innate Lymphoid Cells and Colonic Inflammation

AU - Emgård, Johanna

AU - Kammoun, Hana

AU - García-Cassani, Bethania

AU - Chesné, Julie

AU - Parigi, Sara M

AU - Jacob, Jean-Marie

AU - Cheng, Hung-Wei

AU - Evren, Elza

AU - Das, Srustidhar

AU - Czarnewski, Paulo

AU - Sleiers, Natalie

AU - Melo-Gonzalez, Felipe

AU - Kvedaraite, Egle

AU - Svensson, Mattias

AU - Scandella, Elke

AU - Hepworth, Matthew R

AU - Huber, Samuel

AU - Ludewig, Burkhard

AU - Peduto, Lucie

AU - Villablanca, Eduardo J

AU - Veiga-Fernandes, Henrique

AU - Pereira, João P

AU - Flavell, Richard A

AU - Willinger, Tim

N1 - Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.

PY - 2018/1/16

Y1 - 2018/1/16

N2 - Group 3 innate lymphoid cells (ILC3s) sense environmental signals and are critical for tissue integrity in the intestine. Yet, which signals are sensed and what receptors control ILC3 function remain poorly understood. Here, we show that ILC3s with a lymphoid-tissue-inducer (LTi) phenotype expressed G-protein-coupled receptor 183 (GPR183) and migrated to its oxysterol ligand 7α,25-hydroxycholesterol (7α,25-OHC). In mice lacking Gpr183 or 7α,25-OHC, ILC3s failed to localize to cryptopatches (CPs) and isolated lymphoid follicles (ILFs). Gpr183 deficiency in ILC3s caused a defect in CP and ILF formation in the colon, but not in the small intestine. Localized oxysterol production by fibroblastic stromal cells provided an essential signal for colonic lymphoid tissue development, and inflammation-induced increased oxysterol production caused colitis through GPR183-mediated cell recruitment. Our findings show that GPR183 promotes lymphoid organ development and indicate that oxysterol-GPR183-dependent positioning within tissues controls ILC3 activity and intestinal homeostasis.

AB - Group 3 innate lymphoid cells (ILC3s) sense environmental signals and are critical for tissue integrity in the intestine. Yet, which signals are sensed and what receptors control ILC3 function remain poorly understood. Here, we show that ILC3s with a lymphoid-tissue-inducer (LTi) phenotype expressed G-protein-coupled receptor 183 (GPR183) and migrated to its oxysterol ligand 7α,25-hydroxycholesterol (7α,25-OHC). In mice lacking Gpr183 or 7α,25-OHC, ILC3s failed to localize to cryptopatches (CPs) and isolated lymphoid follicles (ILFs). Gpr183 deficiency in ILC3s caused a defect in CP and ILF formation in the colon, but not in the small intestine. Localized oxysterol production by fibroblastic stromal cells provided an essential signal for colonic lymphoid tissue development, and inflammation-induced increased oxysterol production caused colitis through GPR183-mediated cell recruitment. Our findings show that GPR183 promotes lymphoid organ development and indicate that oxysterol-GPR183-dependent positioning within tissues controls ILC3 activity and intestinal homeostasis.

KW - Animals

KW - Cell Movement

KW - Colitis

KW - Colon

KW - Cytokines

KW - Flow Cytometry

KW - Fluorescent Antibody Technique

KW - Ligands

KW - Lymphocytes

KW - Lymphoid Tissue

KW - Mice

KW - Oxysterols

KW - Real-Time Polymerase Chain Reaction

KW - Receptors, G-Protein-Coupled

KW - Signal Transduction

KW - Journal Article

KW - Research Support, N.I.H., Extramural

KW - Research Support, Non-U.S. Gov't

U2 - 10.1016/j.immuni.2017.11.020

DO - 10.1016/j.immuni.2017.11.020

M3 - SCORING: Journal article

C2 - 29343433

VL - 48

SP - 120

EP - 132

JO - IMMUNITY

JF - IMMUNITY

SN - 1074-7613

IS - 1

ER -