Vitamin D Inhibits IL-22 Production Through a Repressive Vitamin D Response Element in the il22 Promoter
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Vitamin D Inhibits IL-22 Production Through a Repressive Vitamin D Response Element in the il22 Promoter. / Lopez, Daniel V.; Al-Jaberi, Fatima A.H.; Damas, Nkerorema D.; Weinert, Brian T.; Pus, Urska; Torres-Rusillo, Sara; Woetmann, Anders; Ødum, Niels; Bonefeld, Charlotte M.; Kongsbak-Wismann, Martin; Geisler, Carsten.
In: Frontiers in Immunology, Vol. 12, 715059, 2021.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Vitamin D Inhibits IL-22 Production Through a Repressive Vitamin D Response Element in the il22 Promoter
AU - Lopez, Daniel V.
AU - Al-Jaberi, Fatima A.H.
AU - Damas, Nkerorema D.
AU - Weinert, Brian T.
AU - Pus, Urska
AU - Torres-Rusillo, Sara
AU - Woetmann, Anders
AU - Ødum, Niels
AU - Bonefeld, Charlotte M.
AU - Kongsbak-Wismann, Martin
AU - Geisler, Carsten
N1 - Publisher Copyright: © Copyright © 2021 Lopez, Al-Jaberi, Damas, Weinert, Pus, Torres-Rusillo, Woetmann, Ødum, Bonefeld, Kongsbak-Wismann and Geisler.
PY - 2021
Y1 - 2021
N2 - Th22 cells constitute a recently described CD4+ T cell subset defined by its production of interleukin (IL)-22. The action of IL-22 is mainly restricted to epithelial cells. IL-22 enhances keratinocyte proliferation but inhibits their differentiation and maturation. Dysregulated IL-22 production has been associated to some inflammatory skin diseases such as atopic dermatitis and psoriasis. How IL-22 production is regulated in human T cells is not fully known. In the present study, we identified conditions to generate Th22 cells that do not co-produce IL-17 from naïve human CD4+ T cells. We show that in addition to the transcription factors AhR and RORγt, the active form of vitamin D3 (1,25(OH)2D3) regulates IL-22 production in these cells. By studying T cells with a mutated vitamin D receptor (VDR), we demonstrate that the 1,25(OH)2D3-induced inhibition of il22 gene transcription is dependent on the transcriptional activity of the VDR in the T cells. Finally, we identified a vitamin D response element (VDRE) in the il22 promoter and demonstrate that 1,25(OH)2D3-VDR directly inhibits IL-22 production via this repressive VDRE.
AB - Th22 cells constitute a recently described CD4+ T cell subset defined by its production of interleukin (IL)-22. The action of IL-22 is mainly restricted to epithelial cells. IL-22 enhances keratinocyte proliferation but inhibits their differentiation and maturation. Dysregulated IL-22 production has been associated to some inflammatory skin diseases such as atopic dermatitis and psoriasis. How IL-22 production is regulated in human T cells is not fully known. In the present study, we identified conditions to generate Th22 cells that do not co-produce IL-17 from naïve human CD4+ T cells. We show that in addition to the transcription factors AhR and RORγt, the active form of vitamin D3 (1,25(OH)2D3) regulates IL-22 production in these cells. By studying T cells with a mutated vitamin D receptor (VDR), we demonstrate that the 1,25(OH)2D3-induced inhibition of il22 gene transcription is dependent on the transcriptional activity of the VDR in the T cells. Finally, we identified a vitamin D response element (VDRE) in the il22 promoter and demonstrate that 1,25(OH)2D3-VDR directly inhibits IL-22 production via this repressive VDRE.
KW - IL-17
KW - IL-22
KW - Th22 cells
KW - vitamin D
KW - vitamin D receptor
KW - vitamin D response element (VDRE)
U2 - 10.3389/fimmu.2021.715059
DO - 10.3389/fimmu.2021.715059
M3 - Journal article
C2 - 34408754
AN - SCOPUS:85112743971
VL - 12
JO - Frontiers in Immunology
JF - Frontiers in Immunology
SN - 1664-3224
M1 - 715059
ER -
ID: 276651959