Frontiers in immunology · 2026
Tissue-resident memory T cells in atopic dermatitis: mechanisms of residual inflammation, relapse, and therapeutic persistence.
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Zdanowska Natalia, Machoń Natalia, Frączek Alicja, Kasprowicz-Furmańczyk Marta, Czerwińska Joanna, Owczarczyk-Saczonek Agnieszka
Аннотация
BACKGROUND: Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disease in which disease flares frequently recur at previously affected anatomical sites. This distinctive clinical pattern suggests the presence of residual inflammation and long-lasting local immune memory that persists beyond apparent clinical remission.
OBJECTIVES: To synthesize current evidence on the role of tissue-resident memory T (TRM) cells in the pathogenesis, chronicity, and relapse of AD, and to discuss how TRM biology may explain disease recurrence after treatment withdrawal and inform future therapeutic strategies.
METHODS: Narrative review of experimental, translational, and clinical studies addressing TRM differentiation, persistence, metabolic and epigenetic programming, clonal stability, microenvironmental crosstalk, and treatment-related modulation in AD and related chronic dermatoses.
RESULTS: TRM are long-lived, non-circulating T cells retained in the skin through adhesion molecules, survival cytokines, metabolic adaptation, and stable epigenetic programs. In AD, both CD4+ and CD8+ TRM persist in lesional and clinically resolved skin and remain transcriptionally poised for rapid reactivation. Clinical studies consistently demonstrate disease relapse after discontinuation of biologics and JAK inhibitors, supporting the concept that current therapies suppress inflammatory pathways without eliminating pathogenic tissue memory. Emerging data suggest that selected interventions, including modulation of costimulatory pathways and survival signals, may partially influence immune memory and prolong disease control in subsets of patients.
CONCLUSION: TRM constitute a central cellular substrate of residual disease memory in AD and provide a mechanistic explanation for site-specific relapse and treatment resistance. Therapeutic strategies that selectively modulate pathogenic TRM and their supporting microenvironment, while preserving protective barrier immunity, may be required to achieve durable remission.
OBJECTIVES: To synthesize current evidence on the role of tissue-resident memory T (TRM) cells in the pathogenesis, chronicity, and relapse of AD, and to discuss how TRM biology may explain disease recurrence after treatment withdrawal and inform future therapeutic strategies.
METHODS: Narrative review of experimental, translational, and clinical studies addressing TRM differentiation, persistence, metabolic and epigenetic programming, clonal stability, microenvironmental crosstalk, and treatment-related modulation in AD and related chronic dermatoses.
RESULTS: TRM are long-lived, non-circulating T cells retained in the skin through adhesion molecules, survival cytokines, metabolic adaptation, and stable epigenetic programs. In AD, both CD4+ and CD8+ TRM persist in lesional and clinically resolved skin and remain transcriptionally poised for rapid reactivation. Clinical studies consistently demonstrate disease relapse after discontinuation of biologics and JAK inhibitors, supporting the concept that current therapies suppress inflammatory pathways without eliminating pathogenic tissue memory. Emerging data suggest that selected interventions, including modulation of costimulatory pathways and survival signals, may partially influence immune memory and prolong disease control in subsets of patients.
CONCLUSION: TRM constitute a central cellular substrate of residual disease memory in AD and provide a mechanistic explanation for site-specific relapse and treatment resistance. Therapeutic strategies that selectively modulate pathogenic TRM and their supporting microenvironment, while preserving protective barrier immunity, may be required to achieve durable remission.