Immune mechanisms in oral lichen planus.
Although we still don't know the cause, there has been much research into the immune and pathological mechanisms that underlie oral lichen planus (OLP) and it is now possible to piece together a much clearer picture of the disease process. There is consensus that in OLP there is chronic, cell-mediated, immune damage to basal keratinocytes in the oral mucosa that are recognized as being antigenically foreign or altered. In most cases, however, the identity of the target antigen remains unknown. It is likely that cytokines released by the affected keratinocytes, and the associated inflammatory infiltrate, play a key role in the selective recruitment of the T-cell-dominated infiltrate that characterizes OLP, through their ability to induce adhesion molecule expression as well as further cytokine and chemokine release. In susceptible individuals, chronic presentation of antigen by basal keratinocytes may perpetuate the condition and direct cell-mediated immune damage on the keratinocytes.
Thornhill
M H
MH
Oral Disease Research Centre, Bart's and the London, Queen  Mary School of Medicine and Dentistry, UK. M.H.Thornhill@mds.qmw.ac.uk
D017951:Antigen Presentation / Q000276:immunology; D001324:Autoantigens / Q000276:immunology; D015815:Cell Adhesion Molecules / Q000276:immunology; D018925:Chemokines / Q000276:immunology; D016207:Cytokines / Q000276:immunology; D004198:Disease Susceptibility; D006801:Humans; D007111:Immunity, Cellular / Q000276:immunology; D015603:Keratinocytes / Q000276:immunology; D017676:Lichen Planus, Oral / Q000276:immunology*; D009061:Mouth Mucosa / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology
D001324:Autoantigens; D015815:Cell Adhesion Molecules; D018925:Chemokines; D016207:Cytokines