Session Time: 5:30pm-7:30pm
Presentation Time: 5:30pm-7:30pm
Location: Hall 4EF
Introduction: FoxP3+ Treg cells are central in controlling immune responses and transplant tolerance. CD73 (ecto-5'-nucleotidase), which serves to convert AMP to adenosine, is essential for the suppressive activity of FoxP3+ Treg cells. Recent studies identified that aryl hydrocarbon receptor (AhR) regulates Treg and Th17 cell differentiation in a ligand-specific manner, as ITE promotes Treg development while FICZ favors Th17 polarization. Galangin, a natural flavonol, is known to activate AhR signal pathways with anti-inflammatory properties. In this study, we examined whether and how Galangin may affect Treg development and have immunosuppressive functions.
Methods: Naïve CD4+ T cells isolated from wild type C57BL/6 mice were activated with plate-bound anti-CD3 (5[mu]g/ml) and soluble anti-CD28 (1[mu]g/ml), with or without Galangin (10[mu]M). For Treg and Th17 development, the cells were stimulated with TGFβ (10ng/ml) and TGFβ plus IL-6 (20ng/ml), respectively, with or without Galangin. After 72 hours, FoxP3, CD73 and IL-17 expressions were measured by quantitative real-time RT-PCR.
Results: Galangin alone induced FoxP3 expression in CD4+ T cells . Under conditions of Treg differentiation, Galangin enhanced TGFβ-mediated FoxP3 and CD73 induction, and also significantly increased FoxP3 while suppressed IL-17 expression under Th17 polarizing conditions.
Conclusion: Galangin promotes FoxP3 expression and Treg development and function, therefore could be explored as a potential immunosuppressive reagent for transplantation.
CITATION INFORMATION: Liang F., Fang H., Zhang R., Chen Q., Ochando J., Ding Y., Xu J. Galangin Promotes Treg Development and Function Am J Transplant. 2017;17 (suppl 3).
To cite this abstract in AMA style:Liang F, Fang H, Zhang R, Chen Q, Ochando J, Ding Y, Xu J. Galangin Promotes Treg Development and Function [abstract]. https://atcmeetingabstracts.com/abstract/galangin-promotes-treg-development-and-function/. Accessed April 24, 2019.
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