Sugerman P B, Savage N W, Walsh L J, Seymour G J
Department of Dentistry, University of Queensland, St Lucia, Brisbane, Australia.
Australas J Dermatol. 1993;34(2):63-9. doi: 10.1111/j.1440-0960.1993.tb00860.x.
Current evidence for the involvement of cell-mediated immunological mechanisms in the pathogenesis of oral lichen planus is reviewed. Both a spatial and temporal relationship between cytotoxic T Lymphocytes and epithelial damage have been reported. Although keratinocytes appear to be the target for destruction in oral lichen planus, their role in antigen presentation is unclear. We propose that in oral lichen planus patients, diverse exogenous agents such as drugs, trauma and infection, stimulate the expression of a common self molecule by oral mucosal keratinocytes. An autoimmune reaction by cytotoxic T lymphocytes to these activated keratinocytes may result in the tissue destruction which is characteristic of oral lichen planus.
本文综述了目前关于细胞介导的免疫机制参与口腔扁平苔藓发病机制的证据。细胞毒性T淋巴细胞与上皮损伤之间已被报道存在空间和时间上的关系。虽然角质形成细胞似乎是口腔扁平苔藓中被破坏的靶细胞，但其在抗原呈递中的作用尚不清楚。我们提出，在口腔扁平苔藓患者中，多种外源性因素如药物、创伤和感染，可刺激口腔黏膜角质形成细胞表达一种共同的自身分子。细胞毒性T淋巴细胞对这些活化的角质形成细胞的自身免疫反应可能导致口腔扁平苔藓特有的组织破坏。
