ArticleMicrocirculation (New York, N.Y. : 1994)2025
Regulatory T Cells Control Vascular Adhesion Molecule Expression in Skin Under Inflammatory and Homeostatic Conditions.
Article in Microcirculation (New York, N.Y. : 1994), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Endothelial system dysregulation underlies keloid development and therapeutic targeting.Frontiers in cell and developmental biology · 2026Review
- Regulatory T Cells Control Vascular Adhesion Molecule Expression in Skin Under Inflammatory and Homeostatic Conditions.Microcirculation (New York, N.Y. : 1994) · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
objectiveDuring skin inflammation, inhibition of adhesion of regulatory T cells (Tregs) to the dermal microvascular endothelium leads to exacerbation of inflammation, evidence that the dermal endothelium is a key target of the anti-inflammatory actions of Tregs. The aim of this study was to investigate the capacity of Tregs to control the expression of endothelial adhesion molecules in inflamed and resting skin.
methodsTreg function was assessed in a two-challenge contact hypersensitivity (CHS) model, measuring dermal adhesion molecule expression via imaging of cleared skin. Treg depletion was achieved using Foxp3
resultsCHS induced upregulation of E-selectin and ICAM-1 but not P-selectin and VCAM-1. Elimination of Tregs following CHS challenge resulted in exacerbated skin inflammation and enhanced expression of E-selectin, P-selectin and ICAM-1 in the dermal microvasculature. Multiphoton imaging revealed that at this phase of the response, Tregs were enriched near blood vessels and underwent dynamic migration adjacent to the microvasculature. Additionally, in skin that was not undergoing hapten challenge, absence of Tregs also resulted in upregulation of E-selectin and ICAM-1 in skin vessels.
conclusionsThese observations demonstrate that the microvascular endothelium is a target of the anti-inflammatory actions of Tregs in the skin, both during CHS and in steady-state skin.
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Registered trials
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