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Regulatory T Cells Control Vascular Adhesion Molecule Expression in Skin Under Inflammatory and Homeostatic
M Ursula Norman1, Brandon Lim1, Lucinda Jenkins1
1Centre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, Clayton, Victoria, Australia.
Microcirculation (New York, N.Y. : 1994)
|June 29, 2025
Summary
Regulatory T cells (Tregs) control skin inflammation by targeting the dermal endothelium. Their absence exacerbates inflammation and alters adhesion molecule expression in both inflamed and resting skin.
Area of Science:
- Immunology
- Dermatology
- Vascular Biology
Background:
- Regulatory T cells (Tregs) are crucial for immune homeostasis and preventing excessive inflammation.
- The dermal endothelium plays a key role in regulating immune cell trafficking during skin inflammation.
- Previous studies suggest Tregs inhibit Treg-endothelial adhesion, exacerbating inflammation.
Purpose of the Study:
- To investigate the role of Tregs in controlling endothelial adhesion molecule expression in the skin.
- To determine if Tregs target inflamed and resting dermal endothelium.
Main Methods:
- Utilized a two-challenge contact hypersensitivity (CHS) mouse model.
- Assessed dermal adhesion molecule expression using imaging of cleared skin.
- Depleted Tregs using Foxp3DTR mice.
Main Results:
- Contact hypersensitivity (CHS) upregulated E-selectin and ICAM-1.
- Treg depletion after CHS exacerbated inflammation and increased E-selectin, P-selectin, and ICAM-1 expression.
- Tregs were observed near dermal blood vessels, migrating dynamically.
- Treg absence in non-inflamed skin also upregulated E-selectin and ICAM-1.
Conclusions:
- The dermal microvascular endothelium is a direct target of Treg anti-inflammatory actions.
- Tregs regulate endothelial adhesion molecules in both inflamed and steady-state skin conditions.
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