Author
Listed:
- 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)
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.
Suggested Citation
Ada Yeste & Ivan D. Mascanfroni & Meghan Nadeau & Evan J. Burns & Ann-Marcia Tukpah & Andrezza Santiago & Chuan Wu & Bonny Patel & Deepak Kumar & Francisco J Quintana, 2014.
"IL-21 induces IL-22 production in CD4+ T cells,"
Nature Communications, Nature, vol. 5(1), pages 1-13, September.
Handle:
RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms4753
DOI: 10.1038/ncomms4753
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