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Abstract B146: The tumor necrosis factor superfamily member RANKL suppresses effector cytokine production in group 3 innate lymphoid cells

Jennifer Kaoru Bando, Susan Gilfillan, Christina Song, Keely McDonald, Stanley C-C. Huang, Rodney D. Newberry, Yasuhiro Kobayashi, David S.J. Allan, James R. Carlyle, Marina Cella and Marco Colonna
Jennifer Kaoru Bando
Washington University in St. Louis, Saint Louis, MO; Case Western Reserve University of Medicine, Cleveland, OH; Matsumoto Dental University, Shiojiri, Japan; National Institutes of Health, Bethesda, MD; University of Toronto, Toronto, Canada.
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Susan Gilfillan
Washington University in St. Louis, Saint Louis, MO; Case Western Reserve University of Medicine, Cleveland, OH; Matsumoto Dental University, Shiojiri, Japan; National Institutes of Health, Bethesda, MD; University of Toronto, Toronto, Canada.
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Christina Song
Washington University in St. Louis, Saint Louis, MO; Case Western Reserve University of Medicine, Cleveland, OH; Matsumoto Dental University, Shiojiri, Japan; National Institutes of Health, Bethesda, MD; University of Toronto, Toronto, Canada.
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Keely McDonald
Washington University in St. Louis, Saint Louis, MO; Case Western Reserve University of Medicine, Cleveland, OH; Matsumoto Dental University, Shiojiri, Japan; National Institutes of Health, Bethesda, MD; University of Toronto, Toronto, Canada.
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Stanley C-C. Huang
Washington University in St. Louis, Saint Louis, MO; Case Western Reserve University of Medicine, Cleveland, OH; Matsumoto Dental University, Shiojiri, Japan; National Institutes of Health, Bethesda, MD; University of Toronto, Toronto, Canada.
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Rodney D. Newberry
Washington University in St. Louis, Saint Louis, MO; Case Western Reserve University of Medicine, Cleveland, OH; Matsumoto Dental University, Shiojiri, Japan; National Institutes of Health, Bethesda, MD; University of Toronto, Toronto, Canada.
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Yasuhiro Kobayashi
Washington University in St. Louis, Saint Louis, MO; Case Western Reserve University of Medicine, Cleveland, OH; Matsumoto Dental University, Shiojiri, Japan; National Institutes of Health, Bethesda, MD; University of Toronto, Toronto, Canada.
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David S.J. Allan
Washington University in St. Louis, Saint Louis, MO; Case Western Reserve University of Medicine, Cleveland, OH; Matsumoto Dental University, Shiojiri, Japan; National Institutes of Health, Bethesda, MD; University of Toronto, Toronto, Canada.
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James R. Carlyle
Washington University in St. Louis, Saint Louis, MO; Case Western Reserve University of Medicine, Cleveland, OH; Matsumoto Dental University, Shiojiri, Japan; National Institutes of Health, Bethesda, MD; University of Toronto, Toronto, Canada.
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Marina Cella
Washington University in St. Louis, Saint Louis, MO; Case Western Reserve University of Medicine, Cleveland, OH; Matsumoto Dental University, Shiojiri, Japan; National Institutes of Health, Bethesda, MD; University of Toronto, Toronto, Canada.
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Marco Colonna
Washington University in St. Louis, Saint Louis, MO; Case Western Reserve University of Medicine, Cleveland, OH; Matsumoto Dental University, Shiojiri, Japan; National Institutes of Health, Bethesda, MD; University of Toronto, Toronto, Canada.
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DOI: 10.1158/2326-6074.CRICIMTEATIAACR18-B146 Published February 2019
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Abstracts: Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 30 - October 3, 2018; New York, NY

Abstract

While signals that activate group 3 innate lymphoid cells (ILC3s) have been described, the factors that negatively regulate these cells are less well understood. Here we found that the tumor necrosis factor (TNF) superfamily member receptor activator of nuclear factor κB ligand (RANKL) suppressed ILC3 activity in the intestine. Deletion of RANKL in ILC3s and T-cells increased C-C motif chemokine receptor 6 (CCR6)+ ILC3 abundance and enhanced production of interleukin-17A (IL-17A) and IL-22 in response to IL-23 and during infection with the enteric murine pathogen Citrobacter rodentium. Additionally, CCR6+ ILC3s produced higher amounts of the master transcriptional regulator RORγt at steady state in the absence of RANKL. RANKL-mediated suppression was independent of T-cells, and instead occurred via interactions between CCR6+ ILC3s that expressed both RANKL and its receptor, RANK. Thus, RANK-RANKL interactions between ILC3s regulate ILC3 abundance and activation, suggesting that cell clustering may control ILC3 activity.

Citation Format: Jennifer Kaoru Bando, Susan Gilfillan, Christina Song, Keely McDonald, Stanley C-C. Huang, Rodney D. Newberry, Yasuhiro Kobayashi, David S.J. Allan, James R. Carlyle, Marina Cella, Marco Colonna. The tumor necrosis factor superfamily member RANKL suppresses effector cytokine production in group 3 innate lymphoid cells [abstract]. In: Proceedings of the Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; Sept 30-Oct 3, 2018; New York, NY. Philadelphia (PA): AACR; Cancer Immunol Res 2019;7(2 Suppl):Abstract nr B146.

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Cancer Immunology Research: 7 (2 Supplement)
February 2019
Volume 7, Issue 2 Supplement
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Abstract B146: The tumor necrosis factor superfamily member RANKL suppresses effector cytokine production in group 3 innate lymphoid cells
Jennifer Kaoru Bando, Susan Gilfillan, Christina Song, Keely McDonald, Stanley C-C. Huang, Rodney D. Newberry, Yasuhiro Kobayashi, David S.J. Allan, James R. Carlyle, Marina Cella and Marco Colonna
Cancer Immunol Res February 1 2019 (7) (2 Supplement) B146; DOI: 10.1158/2326-6074.CRICIMTEATIAACR18-B146

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Abstract B146: The tumor necrosis factor superfamily member RANKL suppresses effector cytokine production in group 3 innate lymphoid cells
Jennifer Kaoru Bando, Susan Gilfillan, Christina Song, Keely McDonald, Stanley C-C. Huang, Rodney D. Newberry, Yasuhiro Kobayashi, David S.J. Allan, James R. Carlyle, Marina Cella and Marco Colonna
Cancer Immunol Res February 1 2019 (7) (2 Supplement) B146; DOI: 10.1158/2326-6074.CRICIMTEATIAACR18-B146
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