Upregulated KRT17 Promotes Immune Regulation In Oral Lichen Planus

In oral lichen planus (OLP), epithelial damage and aberrant protein expression may trigger immune responses. This study investigated the role of KRT17 in OLP pathogenesis and its impact on CD8⁺ T cell activity. Epithelial cells profiles were analyzed by single-cell RNA sequencing (scRNA-seq) from two non-erosive OLP (NEOLP), two erosive OLP (EOLP), and one healthy control (HC). KRT17 expression was assessed via immunohistochemistry in 20 NEOLP, 23 EOLP, and 18 HC tissues, and then analyzed by Spearman analysis for correlation with OLP clinical severity scores. Peripheral blood mononuclear cells (PBMCs) from 20 NEOLP and 20 EOLP patients were stimulated with recombinant KRT17 to evaluate CD8⁺ T cell percentage and proliferation via flow cytometry and interferon-γ (IFN-γ) secretion via enzyme linked immunosorbent assay (ELISA). Bulk RNA-seq data from 40 OLP samples were analyzed for correlations between KRT17 expression and immune infiltration. KRT17 was significantly upregulated across epithelial subsets. KRT17 expression was elevated in OLP tissues than HC (p < 0.001), and positively associated with REU scores (r = 0.305, p < 0.05). KRT17 protein stimulation increased CD8⁺ T cell counts (p < 0.05) and IFN-γ secretion (p < 0.05) in OLP PBMCs. Positive correlation was confirmed between KRT17 and CD8⁺ T cell infiltration by CYBERSORT (r = 0.410, p < 0.05). KRT17 is upregulated in OLP epithelial cells, and may promote CD8⁺ T cell proliferation and IFN-γ secretion, thereby contributing to immune inflammatory infiltration in OLP.