June 2023
Volume 64, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2023
Treating experimental autoimmune uveitis by regulating Th1 and Th17 sub-populations with green tea extract
Author Affiliations & Notes
  • Bo Man Ho
    The Department of Ophthalmology & Visual Sciences, The Chinese University of Hong Kong, Hong Kong, Hong Kong
  • Lin DU
    The Department of Ophthalmology & Visual Sciences, The Chinese University of Hong Kong, Hong Kong, Hong Kong
  • Sun On Chan
    School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, Hong Kong
  • Calvin C P Pang
    The Department of Ophthalmology & Visual Sciences, The Chinese University of Hong Kong, Hong Kong, Hong Kong
  • WAI KIT CHU
    The Department of Ophthalmology & Visual Sciences, The Chinese University of Hong Kong, Hong Kong, Hong Kong
  • Footnotes
    Commercial Relationships   Bo Man Ho None; Lin DU None; Sun On Chan None; Calvin Pang None; WAI KIT CHU None
  • Footnotes
    Support  United College Early Career Research Excellence Award (2019 to W.K.C); General Research Fund, Research Grants Council, Hong Kong (14104621 and 14102522 to W.K.C.); The Chinese University of Hong Kong Direct Grant (2020.067 and 2021.046 to W.K.C).
Investigative Ophthalmology & Visual Science June 2023, Vol.64, 4375. doi:
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      Bo Man Ho, Lin DU, Sun On Chan, Calvin C P Pang, WAI KIT CHU; Treating experimental autoimmune uveitis by regulating Th1 and Th17 sub-populations with green tea extract. Invest. Ophthalmol. Vis. Sci. 2023;64(8):4375.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : Green tea extract (GTE) has been identified to alleviate the experimental autoimmune uveitis (EAU) animal model by suppressing pathogenic T helper 1 (Th1) and T helper 17 (Th17) cell-related gene expression. Epigallocatechin-3-gallate (EGCG), a major active catechin in green tea, was also proven to impede Th1 and Th17 differentiation and impose an anti-inflammatory effect. Therefore, we aimed to investigate the treatment effects on autoimmune uveitis and the modulating mechanisms of GTE towards Th1 and Th17.

Methods : 6-8-week old C57BL/6 mice were induced with EAU and were fed with 13 doses of GTE throughout the disease induction period. EAU was evaluated by clinical examination using fundus imaging and confocal scanning laser ophthalmoscopy. Compared to the baseline before EAU induction, fold change of retinal-choroidal thickness (RCT) was quantified based on the in vivo measurement by optical coherence tomography. Infiltrated cells from eyes were purified for flow cytometry 21 days after EAU induction to determine the abundance of T cell sub-populations. In addition, naïve CD4+ T cells isolated from healthy murine lymphoid organs were in vitro differentiated into Th1 and Th17 lineages under GTE co-treatment. The effects of GTE towards Th1 and Th17 differentiation were determined by flow cytometry. Data were analysed with two-tailed Student’s t-test and one-way ANOVA, and presented as mean ± standard error of mean.

Results : GTE oral treatment significantly attenuated the clinical manifestations and the average fold change of RCT compared with EAU mice treated with water (Figure. 1a-d). Reduced percentages of Th1, Th17, and pathogenic T cells in eyes were detected by flow cytometry analyses (Figure. 1e-g). In vitro analyses further revealed that GTE impeded Th1 and Th17 differentiation in a dose-dependent manner (Figure. 2).

Conclusions : GTE is a potent agent for alleviating EAU-induced intraocular inflammation by reducing the amount of infiltrating Th1 and Th17 cells. The impeded differentiation in GTE-treated Th1 and Th17 could explain the mechanism of GTE in suppressing autoimmune uveitis.

This abstract was presented at the 2023 ARVO Annual Meeting, held in New Orleans, LA, April 23-27, 2023.

 

Clinical manifestations and retinal-choroidal thickness of GTE-treated EAU mice, and in vivo Th1, Th17, and pathogenic T cell distribution in GTE-treated EAU mice eyes. (*: p≤0.05)

Clinical manifestations and retinal-choroidal thickness of GTE-treated EAU mice, and in vivo Th1, Th17, and pathogenic T cell distribution in GTE-treated EAU mice eyes. (*: p≤0.05)

 

In vitro Th1 and Th17 differentiation under GTE co-treatment. (*: p≤0.05; **: p≤0.01; ***: p≤0.001; ****: p≤0.0001)

In vitro Th1 and Th17 differentiation under GTE co-treatment. (*: p≤0.05; **: p≤0.01; ***: p≤0.001; ****: p≤0.0001)

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