Possible Association between Th1 Immune Polarization and Epithelial Permeability with Toll-Like Receptors 2 Dysfunction in the Pathogenesis of the Recurrent Aphthous Ulceration
The Disease Model of RAU. The genetic background of RAU carriers favors Th1 polarization of the immune reaction (A). A combination of endogenous and exogenous factors that enhances the Th1/Th2 imbalance (B) and augments permeability of the oral mucosa (C) facilitates contact of immune competent cells from the lamina propria with oral antigens or with released host proteins in a milieu rich in Th1 cytokines; this likely influences the onset and outcome of RAU. Conditions that enhance the Th2 immune response (D), diminish epithelium permeability (E), or augment peripheral tolerance (F and G), such as IL-10, TGF-β, and CD4+CD25+, may counteract Th1/Th2 disruption, thus aiding in either the prevention of RAU onset or ameliorating its outcomes. The production of CD4+CD25+ cells is probably inversely proportional to Th17 cells (G), which could potentially influence the induction and maintenance of the inflammatory reaction.