Memory Cells in Atopic Dermatitis: Paving the Way to Disease Modification - PubMed
3 hours ago
- #Immunological Memory
- #Atopic Dermatitis
- #Type 2 Inflammation
- Atopic dermatitis (AD) is a chronic inflammatory skin disease with immunological memory contributing to recurrence and progression.
- Pathogenic tissue-resident memory T cells (TRM) persist in skin and produce cytokines like IL-4, IL-13, IL-22, and IL-31, driving inflammation and barrier dysfunction.
- Circulating CLA+ memory T cells and type-2 memory B cells (MBC2) contribute to flare reactivation and IgE production, linking skin inflammation with allergies.
- Epithelial alarmins, dendritic cell-derived chemokines (CCL17, CCL22, CCL18), and the OX40/OX40L pathway sustain adaptive memory compartments.
- IL-4/IL-13 blockade reduces circulating type-2 responses, but Th2A cells, Tc2 cells, and dendritic cells persist in resolved skin, leading to relapse.
- Targeting memory-imprinting pathways may offer durable disease modification in AD.