Pathology, research and practice · 2026
A novel role for RAC2 in keratinocyte inflammation and dysfunction in oral lichen planus.
СтатьяНазвание и аннотация: Перевод в очереди
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Sen Mu, Huishu Li, Yunfei Xia, Yaping Huang, Jiaqi Kong, Zhuoran Zhang, Qianyang Zhang, Mingxing Wang, Jingru Wang, Xinru Guo, Nan Miao, Ying Yan, Yuanbo Zhan
Аннотация
BACKGROUND AND OBJECTIVE: Oral lichen planus (OLP) is a chronic inflammatory disease characterized by T-cell infiltration and basal keratinocyte apoptosis. The molecular mechanisms linking immune activation to epithelial damage remain elusive. RAC2, a hematopoietically-enriched Rho GTPase, is a key regulator of immune cell functions. However, the relationship between RAC2 and OLP remains unclear. This study aimed to elucidate the precise localization and functional role of RAC2 in OLP pathogenesis.
METHODS: Immunohistochemistry and multiplex immunofluorescence were used to map RAC2 expression in clinical tongue dorsum OLP tissues. An inflammatory model was established in human oral keratinocytes (HOK) using lipopolysaccharide (LPS). The functional consequences of RAC2 expression and knockdown were assessed using qRT-PCR, Western blot, CCK-8, scratch assay, and apoptosis assays.
RESULTS: RAC2 localization differed between groups: in normal controls, it was restricted to the epithelial basal layer; in OLP tissues, it was widely upregulated in both infiltrating CD4 + /CD8 + T cells and epithelial layers (excluding parakeratotic regions). LPS stimulation upregulated RAC2 alongside IL-1β and IL-6 in HOK, impairing cell proliferation/migration and increasing apoptosis. Under basal conditions, RAC2 knockdown impaired HOK proliferation and migration. Notably, under LPS-induced stress, RAC2 knockdown attenuated inflammatory responses (reduced IL-1β/IL-6), decreased apoptosis, and partially restored HOK functional capacities.
CONCLUSION: RAC2 plays a novel dual role in OLP at the immune-epithelial interface, mediating inflammatory responses and regulating keratinocyte function. Targeting RAC2 may offer a strategy to modulate OLP-related epithelial inflammation and impairment.
METHODS: Immunohistochemistry and multiplex immunofluorescence were used to map RAC2 expression in clinical tongue dorsum OLP tissues. An inflammatory model was established in human oral keratinocytes (HOK) using lipopolysaccharide (LPS). The functional consequences of RAC2 expression and knockdown were assessed using qRT-PCR, Western blot, CCK-8, scratch assay, and apoptosis assays.
RESULTS: RAC2 localization differed between groups: in normal controls, it was restricted to the epithelial basal layer; in OLP tissues, it was widely upregulated in both infiltrating CD4 + /CD8 + T cells and epithelial layers (excluding parakeratotic regions). LPS stimulation upregulated RAC2 alongside IL-1β and IL-6 in HOK, impairing cell proliferation/migration and increasing apoptosis. Under basal conditions, RAC2 knockdown impaired HOK proliferation and migration. Notably, under LPS-induced stress, RAC2 knockdown attenuated inflammatory responses (reduced IL-1β/IL-6), decreased apoptosis, and partially restored HOK functional capacities.
CONCLUSION: RAC2 plays a novel dual role in OLP at the immune-epithelial interface, mediating inflammatory responses and regulating keratinocyte function. Targeting RAC2 may offer a strategy to modulate OLP-related epithelial inflammation and impairment.