الفهرس 
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Abstract
Lichen planus is a chronic, inflammatory autoimmune disease of unknown origin. It affects stratified squamous epithelium of oral and genital mucous membranes, skin, nails and scalp. It is characterized by pruritic, violaceous, polygonal, shiny, flat-topped papules and plaques with reticular whitish striae known as Wickham striae.
Currently, the exact pathogenesis of LP remains unclear. Many factors are involved and include, genetic, infectious, metabolic, psychogenic and autoimmune factors. Recent studies reported that LP is a cell-mediated immune disease, triggered by endogenous or exogenous factors, which results in an altered response to autoantigens. In LP lesions, T cells, both CD4+ and CD8+, accumulate in the dermis, whereas CD8+ T cells infiltrate the epidermis. It has been proposed that CD8+ cytotoxic T cells recognize an antigen associated with MHC-I on lesional keratinocytes and lyse them.
Interleukin-18 plays a crucial role in the regulation of Th1 cell differentiation, which induces pro-inflammatory cytokine and chemokine production, such as TNF-α and IFN-γ. Both TNF-α and IFN-γ induce keratinocytes apoptosis which may contribute in pathogenesis of LP. Additionally, IL-18 upregulates both FasL and perforin-dependent cytotoxic effector functions of T and NK cells. Fas ligand induces keratinocytes apoptosis by binding to Fas on the surface of keratinocytes. NK cells and cytotoxic T-cells may also induce keratinocytes apoptosis via the granzyme B/perforin pathway.
Summary