| Autor: |
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 |
| Předmět: |
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| Zdroj: |
Frontiers in Immunology; 8/2/2021, Vol. 12, p1-12, 12p |
| Abstrakt: |
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. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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