Objective To investigate the mechanism of IL-17, the signature cytokine produced by Th17 cells, in OLP lesion. Methods 24 patients with reticular OLP, 19 patients with atrophic-erosive OLP and 13 healthy volunteers were enrolled in this study . Real-time quantitative PCR ( real-time qPCR ) was performed to analyze the expressions of the production of IL-17 and CCL20 mRNA. Results The expressions of IL-17 mRNA in reticular OLP and atrophic-erosive OLP were significant higher than that in healthy oral mucosa (P = 0.0095, P <0.0001, respectively), meanwhile, remarkable increased IL-17 expression in atrophic-erosive OLP group was found compared with reticular OLP group (P = 0.0012). Additionally, the expressions of CCL20 mRNA in reticular OLP and atrophic-erosive OLP were significant higher than that in control group (P=0.0357, P<0.0001, respectively), meanwhile, CCL20 expression in atrophic-erosive OLP was higher than that in reticular OLP. The expressions of CCL20 mRNA rises with the increased expression of IL-17, and were positive correlated with IL-17 expressions in OLP lesions (P=0.003). Conclusions IL-17 production can induce chemokine CCL20 expression in OLP lesion. The signal pathway may promote the migration and infiltration of inflammatory cells in OLP lesions.

Oral lichen planus (OLP) is considered a T cell-mediated autoimmune disease with unknown aetiology. T helper cells appear to play an important role in the pathogenesis of OLP. We investigated the possible role of T helper cells, Th1 and Th17, in the lesions and circulation of patients with OLP. Forty patients with OLP and 15 healthy volunteers were recruited. Double immunofluorescence staining was used to detect Th1 and Th17 cells in the OLP lesions, and intracellular cytokine staining and flow cytometry to evaluate the proportion of Th1 and Th17 cells in peripheral blood. The levels of serum interferon (IFN)-γ and interleukin (IL)-17 were assessed by using an enzyme-linked immunosorbent assay. It was found that Th17 cells, as well as Th1 cells, were present in OLP lesions. The proportion of peripheral Th1 and Th17 cells was significantly increased in patients with OLP. The proportion of Th17 cells in atrophic-erosive OLP was elevated as compared with that in reticular OLP. Serum IL-17 levels in OLP patients were significantly higher than in controls, and those in the atrophic-erosive OLP group were increased as compared with the reticular OLP group. However, the levels of serum IFN-γ were slightly decreased in OLP patients. Our data suggested that Th1 and Th17 cells in the local lesions and peripheral blood may be associated with the pathogenesis of OLP, and that IL-17 may be an important proinflammatory cytokine in OLP. These findings enhance our understanding of OLP pathogenesis.

Oral lichen planus (OLP) is considered a T cell-mediated autoimmune disease with unknown aetiology. T helper cells appear to play an important role in the pathogenesis of OLP. We investigated the possible role of T helper cells, Th1 and Th17, in the lesions and circulation of patients with OLP. Forty patients with OLP and 15 healthy volunteers were recruited. Double immunofluorescence staining was used to detect Th1 and Th17 cells in the OLP lesions, and intracellular cytokine staining and flow cytometry to evaluate the proportion of Th1 and Th17 cells in peripheral blood. The levels of serum interferon (IFN)-γ and interleukin (IL)-17 were assessed by using an enzyme-linked immunosorbent assay. It was found that Th17 cells, as well as Th1 cells, were present in OLP lesions. The proportion of peripheral Th1 and Th17 cells was significantly increased in patients with OLP. The proportion of Th17 cells in atrophic-erosive OLP was elevated as compared with that in reticular OLP. Serum IL-17 levels in OLP patients were significantly higher than in controls, and those in the atrophic-erosive OLP group were increased as compared with the reticular OLP group. However, the levels of serum IFN-γ were slightly decreased in OLP patients. Our data suggested that Th1 and Th17 cells in the local lesions and peripheral blood may be associated with the pathogenesis of OLP, and that IL-17 may be an important proinflammatory cytokine in OLP. These findings enhance our understanding of OLP pathogenesis.
Child ; Female ; Humans ; Interferon-gamma ; immunology ; Interleukin-17 ; immunology ; Lichen Planus, Oral ; immunology ; pathology ; Male ; Middle Aged ; Th1 Cells ; immunology ; Th17 Cells ; immunology

To observe the effects of basic fibroblast growth factor (bFGF) on human adenoid cystic carcinoma ACC-2 cell line proliferation and ERK, cyclin D1/p21waf/ciplsignaling pathways, human adenoid cystic carcinoma cells (ACC-2) were cultured and the influence of bFGF of different concentrations on cell proliferation was determined by MTT. Protein was detected by im muno-precipitation and ERK activity by using ERK agent kit. P-ERK1/2 and down-stream cyclin D1, p21waf/ciplexpression were detected by Western blotting and the interfering role of mitogen pro- tein-activated kinase (MEK) suppressor U0126 in the afore-mentioned indicators was examined. MTr demonstrated ACC-2 cell proliferation was substantially enhanced by bFGF, immuo-precipitation displayed ERK activity was up-regulated by bFGF, and immuno-imprinting also showed p-ERK1/2, cyclin D1 expression was greatly enhanced and p21waf/ciplexpression was inhibited by bFGE U0126 suppressed the effect of bFGE It is concluded that bFGF can promote the proliferation of human adenoid cystic carcinoma ACC-2 cells, and its pathways are associated with the up-regulated activity and expression of p-ERK1/2, inhibited p21waf/cipl expression and enhanced cyclin DI expression.