No abstract

Presented observations confirm that the innate immune system is involved in RAU pathogenesis.

These findings suggest that CD4(+)CD25(high) Treg cells are both functionally and quantitatively compromised in RAS and that decreased constitutive expression of IDO in oral mucosa in RAS may lead to the loss of local immune tolerance.

The pathogenesis of recurrent aphthous ulceration (RAU) is unknown, although an abnormal immune reaction appears to be involved. RAU may result from oral epithelium damage caused by T cell-mediated immune response. To improve understanding of the role of T cells in RAU, the present study analyzed. the expression of T cell-related genes in oral ulcers from patients with RAU, as well as in healthy non-keratinized oral mucosa from aphthae-free volunteers. Biopsies from RAU patients and healthy individuals were analyzed using Human Th1-Th2-Th3 RT(2) Profiler PCR Array and qRT-PCR that allowed to quantify the transcript levels of 86 genes related to T cell activation. We found that cells present in aphthous ulcers express a characteristic Th1-like gene profile. The majority of genes up-regulated in aphthous lesions such as IFN-γ, TNF, IL-15, IRF1, STAT-1 and STAT-4 were Th1-associated. Th2-realated genes were not overexpressed in RAU tissues, with the exception for CCR3. Th3- and Th17-related gene expression patterns were not demonstrated in RAU. These findings clearly reveal that aphthous ulcer formation is predominantly dependent on the activation of the Th1-type immune response.

No abstract