It is becoming increasingly apparent that the tumor microenvironment plays an important role in the progression of cancer. The microenvironment may promote tumor cell survival and proliferation or, alternatively may induce tumor cell apoptosis. Toll-like receptors (TLRs) are transmembrane proteins, expressed on immune cells and epithelial cells, that recognize exogenous and endogenous macromolecules. Once activated, they initiate signaling pathways leading to the release of cytokines and chemokines, which recruit immune cells inducing further cytokine production, the production of angiogenic mediators and growth factors, all of which may influence tumor progression. This paper examines the actions of TLRs in carcinogenesis with particular emphasis on their role in oral squamous cell carcinoma.

The findings indicate that angiogenic factors are differentially expressed in oral lichen planus compared with inflamed controls, with increased expression of pro-angiogenic factors and decreased anti-angiogenic expression.

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Based on the findings of this study, we suggest that the source of low levels of IL17A in periodontal tissues is mast cells not Th17 cells and that Tregs may have a more prominent role in the pathogenesis of periodontal disease than Th17 cells.

Oral lichen planus (OLP) is an immunological disease and while it is understood that the T cell subsets, FoxP3(+) Tregs and IL17(+) Th17 cells are involved in immune regulation, little is known about their presence in OLP. The aims of this study were to compare the number of cells expressing FoxP3 or IL-17 in OLP with non-specifically inflamed oral mucosa and to determine which cell types expressed FoxP3 and/or IL-17 and their distribution. Immunohistochemistry was used to investigate the presence of FoxP3(+) or IL-17(+) cells in 12 control cases and 17 cases of OLP. These results were analysed quantitatively and qualitatively. Double-labelling immunofluorescence (IF) was used to determine the type of cell expressing FoxP3/IL-17 and these results were analysed qualitatively. OLP displayed significantly more FoxP3(+) cells (mean 79.3 vs. 20.6 cells/defined area, p < 0.0001) and fewer IL-17(+) cells (mean 1.05 vs. 3.30 cells/defined area, p = 0.0003) than non-specific inflammatory cases. The majority of FoxP3(+) cells were in the sub-epithelial infiltrate, while IL-17(+) cells were deeper in the stromal tissues. IF showed that FoxP3(+) cells co-localised with T cells, while the IL-17(+) cells did not. These results show that the balance between Tregs and IL-17(+) cells is altered in OLP, thus supporting the proposition that disturbance in local immune regulation is important in the pathogenesis of OLP. The observation that the IL-17(+) cells were mast cells has not previously been reported in OLP and again raises questions about the role of mast cells in this condition.