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In Vivo Augmentation of Gut-Homing Regulatory T Cell Induction
Published on: January 22, 2020
VEGFR2 is selectively expressed by FOXP3high CD4+ Treg.
Hiroyuki Suzuki1, Hideya Onishi, Junji Wada
1Department of Cancer Therapy and Research, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
European Journal of Immunology
|November 11, 2009
Summary
Regulatory T cells (Treg) suppress immune responses. This study identifies vascular endothelial growth factor receptor 2 (VEGFR2) as a marker for highly suppressive FOXP3high Treg, suggesting VEGFR2 as a potential therapeutic target.
Area of Science:
- Immunology
- Cell Biology
- Cancer Research
Background:
- CD25+ FOXP3+CD4+ T cells, known as regulatory T cells (Treg), are crucial for maintaining immune tolerance against tumor antigens.
- High expression of FOXP3 (FOXP3high) in Treg confers potent suppressive activity, even to non-Treg cells.
Purpose of the Study:
- To investigate the selective expression of vascular endothelial growth factor receptor 2 (VEGFR2) on Treg.
- To determine if VEGFR2 expression correlates with the suppressive function of Treg.
Main Methods:
- Flow cytometry analysis of Treg populations.
- Characterization of VEGFR2 expression on FOXP3high and FOXP3low Treg.
- Detection of VEGFR2+ Treg in peripheral blood mononuclear cells (PBMC) and malignant effusions.
Main Results:
- VEGFR2 is selectively expressed on FOXP3high Treg, but not on FOXP3low Treg.
- VEGFR2+ Treg were identified in various tissues, including PBMC and lymphocytes from malignant effusions.
- This finding establishes a distinct phenotype for highly suppressive Treg.
Conclusions:
- VEGFR2 is a novel marker for identifying highly suppressive Treg.
- Targeting VEGFR2 may offer a new strategy for controlling Treg-mediated immunosuppression in conditions like cancer.
- Further research into VEGFR2+ Treg function and therapeutic targeting is warranted.
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