Activated Akt/mTOR-autophagy in local T cells of oral lichen planus

- Akt/mTOR-autophagy was activated in local tissues and T cells of oral lichen planus (OLP).
- LC3B expression level was negatively correlated with the disease severity of OLP.
- The expression of LC3B in nonerosive OLP was higher than that in erosive OLP.

Oral lichen planus (OLP) is a chronic inflammatory disease regulated by T cell-mediated immune response. Autophagy and its major inhibitory pathway Akt/mTOR participate in T cell metabolism and homeostasis, which has been implicated in autoimmune diseases. In this study, the potential involvement of autophagy and its regulatory Akt/mTOR pathway were investigated in local T cells of OLP. The expression of Akt/mTOR pathway and autophagy-related proteins in OLP local lesions, as well as in T cells, were measured by immunohistochemistry and double-labeling immunofluorescence, respectively. Furthermore, the associations of p-Akt, p-mTOR, ULK1, and LC3B expression with RAE scores representing the disease severity of OLP were assessed. The expression of p-Akt, p-mTOR, ULK1, and LC3B in OLP lesions, as well as in local T cells, was significantly increased compared with that in controls. In addition, the level of LC3B was negatively correlated with RAE scores of OLP, and LC3B was higher in nonerosive OLP than erosive ones and controls. Our results suggested that activated Akt/mTOR-autophagy may have a role in the local T cell-mediated immunoregulatory mechanism of OLP. LC3B might be a valuable marker to monitor the disease severity of OLP.