Intracellular Signal Transduction in Oral Keratinocytes and Infiltrated Lymphocytes Obtained from Patients with Oral Lichen Planus-Biochemical Analysis of the Mechanism of Enhanced Cytokine Generation from Keratinocytes and Infiltration of Lymphocytes

对口腔扁平苔藓（OLP）进行免疫生物学检查，结果如下：1)与从完整口腔粘膜获得的口腔角质形成细胞（KC）相比，OLP患者的KC （OLP-KC）普遍含有更多的GM-CSF、lL-6、tnf - α和1l -1 β。2) OLP-KC产生的细胞因子增强了外周血单核细胞（PBMC）的趋化性，并增加了PBMC通过单层血管内皮细胞的迁移。3) OLP-KC上清液激活PBMC，上调PKC活性、1p3和[Ca^<2+>]i水平和蛋白酪氨酸磷酸化。4)相应。粘附分子如CD11a、CD11b、CD18和CD49d在PBMC及其对应的ICAM-1上。OLP-KC上清液使内皮细胞上的vcam - 1和elam - 1表达增加，PBMC迁移的增强依赖于这些粘附分子的表达。5) I{C没有产生细胞因子。大肠杆菌- lps、热（42 - C）和热休克蛋白（65 kDa）肽均能增强。6) KC增强细胞因子生成与PKC活化、蛋白酪氨酸磷酸化和NV-KB活化有关。7) CD14则不然。在KC上表达，并通过CD59介导LPS激活KC。这些结果表明，KC产生的细胞因子通过表达粘附分子诱导PBMC迁移，KC产生的细胞因子的增加可能是由外源刺激（如热量和UPS）引起的。每位OLP患者的刺激物的具体情况以及浸润的PBMC在基底细胞损伤中的作用仍有待进一步阐明。

By immunobiological examination in oral lichen planus (OLP), we obtained following results.1) Compared with oral keratinocytes (KC) obtained from the intact oral mucosae, KC from patients with OLP (OLP-KC) generaled larger amounts of GM-CSF, lL-6, TNF-alpha and 1L-1beta.2) Cytokines generated from OLP-KC enhanced chemotaxis of peripheral blood mononulcear cells (PBMC) and they increased migration of PBMC through monolayered blood vessel endothelial cells.3) Supernatants of OLP-KC activated PBMC, upregulating PKC activity, 1P_3 and [Ca^<2+>]i levels and protein tyrosine phosphorylation.4) Correspondingly. adhesion molecules such as CD11a, CD11b, and CD18 and CD49d on PBMC and their counterparts ICAM-1. VCAM-l and ELAM-I on endothelial cells were more expressed by supernatants of OLP-KC and the enhanced migration of PBMC depended on the expression of these adhesion molecules.5) Cytokine generation by I{C was not. enhanced by metal ions but enhanced by E.coli-LPS and heat (42ﾟC) and heat shock protein (65 kDa) peptide.6) The enhanced cytokine generation from KC was associated with PKC activation, protein tyrosine phosphorylation and NV-KB activation.7) CD14 was not. expressed on KC and activation of KC by LPS was mediated by CD59.These results indicate that cytokines generated from KC induce migration of PBMC through expression of adhesion molecules and that exaggeration of cytokine generation from KC may be induced by extrinsic stimulant such as heat and UPS.Specification of the stimulant in each patient with OLP and the role of infiltrated PBMC in the impairment of the basal cells remain to be clarified in the future.