Frontiers in immunology · 2026
Epigenetic reprogramming in autoimmune and immune-mediated skin disease.
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Bilik Sophie M, Kraft Garrett P, Sharifi Isabella, Hanly-Jorda Fiona M, Antonevich Sarah, Jimenez Joaquin J, Satoh Takashi K
Аннотация
BACKGROUND: Autoimmune skin diseases exhibit chronicity and site-specific relapse that are not fully explained by genetic susceptibility or cytokine signaling alone. Emerging evidence suggests that epigenetic reprogramming of skin-resident immune cells contributes to disease persistence and recurrence.
METHODS: We conducted a structured narrative review of the human literature by searching PubMed for studies published from database inception through March 1, 2026. The literature search was performed between February 1 and March 1, 2026 and focused on epigenetic mechanisms across major autoimmune dermatoses, including DNA methylation, histone modification, chromatin accessibility, non-coding RNA regulation, and emerging single-cell and spatial epigenomic technologies.
RESULTS: Current evidence suggests stable chromatin remodeling in keratinocytes and immune cells, including tissue-resident memory T cells, that persists after clinical resolution and may facilitate rapid disease reactivation. Environmental exposures further reinforce these epigenetic programs, contributing to disease heterogeneity, chronicity, and site-specific relapse.
CONCLUSION: Collectively, these findings are consistent with a model in which autoimmune skin diseases are maintained by maladaptive epigenetic memory. Although causal inference remains limited by the relative scarcity of cell-type-resolved human epigenomic data and the predominance of cross-sectional studies, this framework suggests that achieving durable therapeutic remission may require reprogramming pathogenic chromatin states rather than solely suppressing inflammatory pathways.
METHODS: We conducted a structured narrative review of the human literature by searching PubMed for studies published from database inception through March 1, 2026. The literature search was performed between February 1 and March 1, 2026 and focused on epigenetic mechanisms across major autoimmune dermatoses, including DNA methylation, histone modification, chromatin accessibility, non-coding RNA regulation, and emerging single-cell and spatial epigenomic technologies.
RESULTS: Current evidence suggests stable chromatin remodeling in keratinocytes and immune cells, including tissue-resident memory T cells, that persists after clinical resolution and may facilitate rapid disease reactivation. Environmental exposures further reinforce these epigenetic programs, contributing to disease heterogeneity, chronicity, and site-specific relapse.
CONCLUSION: Collectively, these findings are consistent with a model in which autoimmune skin diseases are maintained by maladaptive epigenetic memory. Although causal inference remains limited by the relative scarcity of cell-type-resolved human epigenomic data and the predominance of cross-sectional studies, this framework suggests that achieving durable therapeutic remission may require reprogramming pathogenic chromatin states rather than solely suppressing inflammatory pathways.