Oral lichen planus (LP) is a common mucosal disorder in which cell mediated immunity is thought to play a major role. In this paper, a unifying hypothesis which attempts to integrate cellular and molecular signals in the local immune response in oral LP is presented. In this model, modified keratinocyte surface antigens are the target for the cytotoxic cell response which characterizes oral LP, whereas mast cells and antigen presenting Langerhans cells are key cellular elements in the evolving lesion. It has been established that mast cell degranulation induces adhesion molecule expression on endothelium which facilitates lymphocyte homing to the tissues. These adhesive interactions between lymphocytes and keratinocytes are postulated to be important determinants in the effector phase of the lesion. Cytokines produced by both lymphocytes and keratinocytes which influence the local immune response could promote chronicity. Accordingly, modulation of immunologic events is a potential therapeutic approach for oral LP.
Previous studies have demonstrated heterogeneity within lesional lymphocytes in drug-related oral lichen planus (D-LP) and idiopathic lichen planus (I-LP). This study examined the phenotype of Langerhans cells (LC) and keratinocytes in non-erosive D-LP and I-LP. In I-LP, keratinocytes expressed HLA-DR antigens whilst LC co-expressed CDIa, MHC Class II and CD4 antigens. The high levels of expression of MHC Class II antigens by LC were maintained during short term organ culture. In I-LP, the epithelium contained occasional CD25+ dendritic cells (putative activated LC). These cell phenotypes are suggestive of cell activation and likely result from local production of gamma interferon. In D-LP, expression of MHC Class II antigens on LC was reduced and no CD25+ cells were detected. The epithelium contained an increased number of CD45RA+ dendritic cells. While no differences between the production of interleukin-1 and interleukin-1 inhibitors by tissue samples could be detected, it is likely that the variations in epithelial cell phenotypes in I-LP and D-LP reflect altered cytokine production.
The nature and distribution of mononuclear cells in 30 non‐ulcerated lesions of oral lichen planus (OLP) was investigated, using an immunoperoxidase technique. Most of the infiltrating cells consisted of a mixture of Leu 2a+ and Leu 3a+/3b+ T cells present in the stroma. This study proved histometrically that the emigration of lymphocytes through subepithelial vessels was not selective for major subsets of T cells and subsequent migration to the epithelium was predominant in suppressor/cytotoxic T cell infiltration. HLA‐DR+/DQ+ monocyte/macrophage and Langerhans cells formed a relatively minor component of the cellular infiltrates, whereas a considerable number of T cells expressed the MHC antigens. Also, the keratinocytes of the epithelium expressed only DR antigens. These results support the concept that LP is associated with lymphokine‐generated inflammation induced by helper/inducer T cells or activated T cells which would include direct basal cell damage or local immunosuppression by suppressor/cytotoxic T cells. Furthermore, this study suggests that monocytes/macrophages and Langerhans cells played a role in antigen presentation, and also that keratinocytes may possess a similar function.
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