ArticleFrontiers in cell and developmental biology2026
Integrative single-cell transcriptomic and epitranscriptomic analysis of the RBM15-m6A-IL10 regulatory axis in psoriatic keratinocytes.
Article in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Psoriasis is a chronic immune-mediated inflammatory skin disorder hallmarked by keratinocyte hyperproliferation and impaired apoptosis. N6-methyladenosine (m6A) RNA modification is emerging as a critical regulator of inflammatory gene expression. RNA-binding motif protein 15 (RBM15), a core m6A methyltransferase complex adaptor, promotes oncogenic processes across tissue types; however, its role in psoriatic keratinocyte biology and its potential regulation of interleukin-10 (IL-10)-a pivotal anti-apoptotic and immunomodulatory cytokine-remain unexplored. Methods: Single-cell RNA sequencing data from a publicly deposited psoriasis dataset (GSE248121; 23,851 cells from two paired libraries) were analyzed using Seurat, Monocle3, CellChat, and pySCENIC. Bulk transcriptomic datasets (GSE54456, GSE30999) were used for cross-dataset validation of RBM15 and IL10 expression. Results: Integrated single-cell analysis resolved 23,851 cells into six principal cell types across psoriatic lesional (PP) and clinically normal (NS) skin. RBM15 was markedly upregulated in psoriatic keratinocytes (log2FC = 1.93 [fold change ≈3.82] ± 0.31 vs. NS; p < 0.001) and correlated inversely with IL10 along keratinocyte pseudotime trajectories (r = -0.52, p < 0.001). Cross-dataset validation confirmed concordant RBM15 upregulation and IL10 downregulation in PP lesions. Mechanistically, RBM15 installed m6A marks at two RRACH motifs in the IL10 3'UTR, promoting YTHDF2-mediated mRNA degradation (half-life reduction 53.3%; p < 0.001) and 62% suppression of IL10 protein. Conclusion: RBM15-driven m6A modification of IL10 mRNA constitutes a previously unrecognized epitranscriptomic mechanism suppressing IL-10-mediated survival signaling in psoriatic keratinocytes. Targeting the RBM15-m6A-IL10 axis represents a mechanistically grounded and potentially tractable therapeutic direction for psoriasis, pending further
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