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Updated: Mar 19, 2026

New Tools to Expand Regulatory T Cells from HIV-1-infected Individuals
Published on: May 30, 2013
Prolyl hydroxylase 3 (PHD3) expression augments the development of regulatory T cells
Yogesh Singh1, Xiaolong Shi1, Shaqiu Zhang2
1Departments of Cardiology, Vascular Medicine and Physiology, Eberhard Karls University of Tubingen, Gmelinstraβe 5, D-72076 Tubingen, Germany.
Abstract:
Regulatory T cells (Tregs) are required for effective immune homeostasis by suppressing harmful immune responses against self-antigens. Transcription factor Foxp3 is required for the development of these cells. How Foxp3 is stabilised and affects Tregs development is still incompletely understood. Previous studies have suggested that hypoxia inducible factor gene HIF-1α negatively influences the development of Tregs and enhances the development of IL-17 producing Th17 cells. In this study, we reveal that prolyl hydroxylase 3 (PHD3), which is a negative regulator of HIF-1α, is upregulated in Tregs and enhances the development of Tregs. The PHD3 inhibitor dimethyl oxalylglycine (DMOG) or siRNAs-PHD3, which upregulates HIF-1α, down-regulated Foxp3 expression, and enhanced the development of Th17 cells. Our observations disclose a novel role of PHD3 in the development of Tregs.
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