Notch signaling pathway regulates IL-22 secretion by CD4+T cells in patients with Vogt-Koyanagi-Harada syndrome
- VernacularTitle:Notch信号通路调控CD4+T细胞分泌IL-22在Vogt-小柳原田综合征中的作用
- Author:
Zhao-Jie Chu
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Author Information
- Publication Type:Journal Article
- Keywords: Vogt-Koyanagi-Harada syndrome; Notch signaling pathway; interleukin-22; CD4+ T lymphocytes
- From: International Eye Science 2019;12(7):1114-1118
- CountryChina
- Language:Chinese
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Abstract:
AIM:To investigate the changes of Notch receptors and interleukin(IL)-22 expression in patients with Vogt-Koyanagi-Harada(VKH)syndrome, and to assess the regulatory activity of Notch signaling to IL-22 production by CD4+ T cells in patients with VKH syndrome.
METHODS: Thirty-five patients with VKH syndrome(including fifteen active VKH and twenty inactive VKH)and twelve healthy controls were enrolled. Plasma was isolated, and CD4+T cells were purified. Notch receptors were investigated by qRT-PCR and Western blot. Plasma IL-22 expression was measured by ELISA. The percentage of Th17 and Th22 cells was investigated by flow cytometry. CD4+T cells, which were purified from active VKH patients, were stimulated with Notch signaling inhibitor DAPT. mRNA expression of transcription factor in CD4+T cells as well as IL-22 secretion by CD4+T cells was investigated.
RESULTS: Notch1-Notch3 in CD4+T cells from active VKH syndrome patients was significantly elevated in comparison with inactive VKH and healthy controls. Plasma IL-22 expression and percentage of Th17 and Th22 was notably increased in active VKH syndrome in comparison with inactive VKH and controls. DAPT stimulation inhibited Notch signaling pathway in CD4+T cells, leading to the down-regulation of AhR mRNA and IL-22 secretion.
CONCLUSION:Notch-AhR-IL-22 signaling pathway might take part in the pathogenesis of VKH syndrome.
- Full text:2019070063.pdf
