Fibroblast-encoded inflammatory memory orchestrates recurrent skin inflammation <i>via </i>NNMT-dependent metabolic remodeling

This study aims to elucidate the molecular mechanisms underlying the recurrence of chronic skin inflammation after treatment withdrawal, with a particular focus on the role of dermal fibroblasts in establishing inflammatory memory. Based on our RNA-seq analysis, we found that fibroblasts acquire a persistent senescence-associated secretory phenotype (SASP) during active inflammation and maintain a pro-inflammatory microenvironment in clinically resolved skin, thereby supporting the differentiation and retention of CD8+CD103+ tissue-resident memory T cells (Trm).