Recent advances on the pathogenesis of oral lichen planus (OLP). The adhesion molecules

Oral Lichen Planus is a chronic inflammatory pathology with not well defined etiology, characterized by an immunoreactivity directed against the keratinocytes of basal layer and mediated by a cellular infiltrate of T-lymphocytes. This immunoreactivity is caused by a modification of basal keratinocytes surface antigens, with activation of antigen-presenting cells allowing the recognition on non-self antigens by CD4 lymphocytes. The migration of T-cells at the sites of the damage and their interactions with leucocytes and keratinocytes represent a key effect of pathogenesis of OLP, and are mediated by specific cell surface adhesion molecules. Recent studies in molecular biology, with the discovery and the definition of cell adhesion receptors, have greatly contributed to clarify the pathogenic mechanism of OLP; these molecules regulate immune functions such as adhesion to endothelial cells, lymphocytes migration into extravasal tissues at the site of immune response and T-cell interactions with target cell antigens. The adhesion molecules have been classified into various families, differing on the basis of their molecular structure: the Immunoglobulin Superfamily (ICAM 1-3, PECAM-1, VCAM-1), the Selectins (ELAM-1, LECAM-1, GMP-140), the Integrins (LEA-1) and others. In this paper, the principal classes of adhesion molecules which are involved in the immune response are described and their importance in the pathogenesis of Lichen Planus is underlined.