Oral lichen planus: immunohistology of mucosal lesions

Abstract

The immunological reaction begins with Langerhans cells activation, which presents an antigen to CD4+ lymphocytes. Those cells through ICAM-1 and LFA-1 promote epithelial destruction. Afterwards, cytokine production, ICAM-1 and VCAM-1 expression can activate CD8+ lymphocytes leading to the chronic form of the disease.

Evaluating the role of tissue microRNA‐27b as a diagnostic marker for oral lichen planus and possible correlation with CD8

“…The increased lesional tissue expression of CD8 in our study confirms the role of T cells in OLP pathogenesis . Previous investigators reported T‐cytotoxic cells as the predominant T‐cell type in OLP lesions, whereas others reported the same for T‐helper cells .…”

Expression of cytokeratins, adhesion and activation molecules in oral ulcers of Behçet's disease

“…No VCAM‐1 expression was found on endothelial cells 17 . ICAM‐1 is known to play an important role in the destruction of the basal keratinocyte layer in OLP lesions; VCAM‐1 appears more highly expressed by T cells in the lamina propria and by endothelial cells in OLP 18 . In our study, VCAM‐1, ICAM‐1 and γδ T‐cell expression were each upregulated in BD samples compared with NOM (Fig.…”

Oral lichen planus, hepatitis C virus, and HIV: No association in a cohort study from an area of high hepatitis C virus endemicity

“…It is likely that the functional immunosuppression because of CD4 deficiency caused by HIV does not allow the triggering of in situ cytotoxic mechanisms leading to OLP. 56 It has, in fact, been recently shown that both antigenspecific and -nonspecific mechanisms are involved in the pathogenesis of OLP. 57 On the other hand, the shorter time elapsed since HCV infection in these patients, as compared with those with communityacquired HCV, may have not yet allowed development of OLP.…”