These data further reveal the pathogenesis of OLP, including (1) the characterization of cellular components involved in the pathogenesis of OLP; (2) SFRP2+ fibroblasts involved in the pathogenesis of OLP by production of pro-inflammatory factors; (3) a subset of SFRP2+ fibroblasts contributing to immune disorder through recruiting immune cells and antigen presenting and processing; (4) the interaction among SFRP2+Wnt5a+ fibroblasts, epithelial cells, and CD8+ T cells contributing to amplifying and maintaining the local immune inflammation. This evidence concerns the gene SFRP2 and oral lichen planus.