Gene Expression Analysis of Oral Lichen Planus

Oral Lichen planus (OLP), a dermatologic keratotic disorder, has a clinical presentation in about 1% of the population. Lesions appear in the oral mucous membranes, on the epidermis, and on cutaneous surfaces of the genitals. The persistent immunologic description for OLP is of an acquired,”adaptive” immune dysfunction with a predominance of CD8+ lymphocytes that initiates “an autoimmune phenomenon”. However, previous studies and standard clinical diagnostic procedure for OLP has indicated several innate immune components are present. These include an accumulation and activation of mast cells, and presence of a type III hypersensitivity reaction with diverse granulocyte activation; deposition of autoantibody and complement and release of an array of chemokines; toll-like receptor factors, and interleukins. Furthermore, oral keratinocytes are modifiers of innate and acquired, immunology which is substantiated by examination of a dense inflammatory lymphocytic infiltrate that bands a hyperplastic “saw tooth”, extension of epithelial rete pegs. Using oral brush cytology we are capable to largely dissociate oral epithelium RNA expression from a confounding inflammatory and stromal expression component. We observed expression of twelve genes but six genes were localized to epithelium in OLP patients: CD14, CXCL1, IL8, ANXA1, ALOX12, and TLR1. Not previously considered is this set of genes that are positive components of the innate immune response and possible targets for treatment. We suggest that OLP eruptions are a product of immune events that begin with innate immunity dysfunctions and become amplified in later acquired immune presentation that leads to a loss of tolerance and synthesis of autoantibody and autoimmune disease.