Regulatory T cells in atopic dermatitis: mechanisms of dysfunction, plasticity and therapeutic reprogramming
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Updated: Nov 6, 2026

Development of Stem Cell-derived Antigen-specific Regulatory T Cells Against Autoimmunity
Published on: November 8, 2016
Shreya Ashok Bhandari1, Priti Kumari1, Mrinmoy Das2
1Division of Medical Research, SRM Medical College Hospital and Research Centre, SRM Institute of Science and Technology, Kattankulathur, Chengalpattu, Tamil Nadu, India.
Objective And Design:
This review focused on current evidence regarding the mechanisms underlying regulatory T cell (Treg) dysfunction in atopic dermatitis (AD), with particular emphasis on Treg instability, tissue microenvironmental reprogramming, inflammatory plasticity, and the skin-gut immune axis, and evaluated Treg-directed therapeutic strategies.
Methods:
Experimental and clinical studies investigating Treg functions, tissue microenvironment, immune regulation, microbial dysbiosis, and therapeutics in AD were critically analysed and integrated into a mechanistic framework.
Results:
AD is a chronic inflammatory skin disease with epidermal barrier dysfunction, pruritus, microbial dysbiosis, and immune dysregulation. Current evidence suggests that Treg abundance, phenotype, localization, and suppressive function may differ across AD endotypes and tissue compartments. Functional impairment or maladaptive plasticity might play a role in persistent inflammation within specific Treg populations. This may link to FOXP3 instability, altered IL-2/STAT5 signaling, metabolic strain, cytokine-induced destabilization, plasticity, keratinocyte-derived alarmins, inflammatory dendritic cells, Staphylococcus aureus colonization, and the skin-gut microbial axis. Novel therapeutics may restore immune tolerance beyond conventional anti-inflammatory treatment, including Treg-selective IL-2 agonists, microbiome-based therapy, and antigen-specific regulatory approaches.
Conclusion:
Treg dysregulation may represent a major component in AD pathogenesis, but its causality for disease persistence and therapeutic reversibility is yet to be elucidated.
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