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IL-21 induces IL-22 production in CD4+ T cells

Ada Yeste, Ivan D. Mascanfroni, Meghan Nadeau, Evan J. Burns, Ann-Marcia Tukpah, Andrezza Santiago, Chuan Wu, Bonny Patel, Deepak Kumar and Francisco J Quintana ()
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Ada Yeste: Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School
Ivan D. Mascanfroni: Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School
Meghan Nadeau: Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School
Evan J. Burns: Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School
Ann-Marcia Tukpah: Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School
Andrezza Santiago: Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School
Chuan Wu: Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School
Bonny Patel: Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School
Deepak Kumar: Biological Chemistry and Molecular Pharmacology, Harvard Medical School
Francisco J Quintana: Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School

Nature Communications, 2014, vol. 5, issue 1, 1-13

Abstract: Abstract Interleukin (IL)-22 produced by innate lymphoid cells (ILCs) and CD4+ T cells plays an important role in host defence and mucosal homeostasis, thus it is important to investigate the mechanisms that regulate IL-22 production. We investigated the regulation IL-22 production by CD4+ T cells. Here we show that IL-21 triggers IL-22, but not IL-17 production by CD4+ T cells. STAT3, activated by IL-21, controls the epigenetic status of the il22 promoter and its interaction with the aryl hydrocarbon receptor (AhR). Moreover, IL-21 and AhR signalling in T cells control IL-22 production and the development of dextran sodium sulphate-induced colitis in ILC-deficient mice. Thus, we have identified IL-21 as an inducer of IL-22 production in CD4+ T cells in vitro and in vivo.

Date: 2014
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms4753

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DOI: 10.1038/ncomms4753

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