INTRODUCTIONOral lichen planus (OLP) is a mucocutaneous T cell‐mediated chronic inflammatory disease of unknown aetiology. Mouth lesions have six clinical presentations, including reticular, papular, plaque‐like, erosive, atrophic and bullous, being the presence of white striae a clinical hallmark of the disease (van der Meij, Schepman, & van der Waal, ; Roopashree et al., ). Microscopically, it is characterised by a dense band‐like subepithelial lymphocytic infiltration and degeneration of basal keratinocytes, in a process orchestrated by T cells (Sugerman et al., ). In this context, cytotoxic CD8+ T cells are observed adjacent to basal keratinocytes and inside the epithelium while CD4+ T cells are shown to be present in the lamina propria. Besides, the lesional epithelium shows a higher concentration of Langerhans cells (LC), which are responsible for processing and presenting antigen derived to T cells and promote its activation (Gueiros et al., ). In this scenario, CD8+ cytotoxic T cells lead to keratinocyte apoptosis and consequent basal membrane disruption in a process regulated by CD4+ T cells through the promotion of an altered cytokine profile (Roopashree et al., ; Xie, Ding, Xiong, & Zhu, ).Recent evidence supports a central role of immune dysregulation in the pathogenesis of OLP (Lu, Zhang, Sun, Du, &
Oral Diseases – Wiley
Published: Jan 1, 2018
Keywords: ; ; ;
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