Interferon-γ activated T-cell IRGM-autophagy axis in oral lichen planus

Oral lichen planus (OLP) is an inflammatory immune disease featured by dense T-cell infiltrate and basal keratinocytes degeneration. Immunity related GTPase M (IRGM) is vital for the induction of autophagy. Our previous studies have demonstrated aberrant autophagy in OLP, however, the involvement of IRGM-autophagy axis in OLP has not yet been revealed. The expression of IRGM and autophagy activity were evaluated in oral mucosal tissues and peripheral T cells of OLP patients and healthy controls, respectively. We found significant upregulation of IRGM and LC3B in lesions of patients with OLP as compared with healthy donors. IRGM, LC3B and NOD2 levels were also elevated in the peripheral T cells of OLP. Then, knockdown of IRGM after electrotransfection with siRNA resulted in attenuated autophagy, growth inhibition, and apoptosis of T cells. In addition, preincubation with IFN-gamma promoted the expression of IRGM mRNA and induced autophagy in T cells. Furthermore, IFN-gamma decreased the proliferation and apoptosis of T cells, whereas facilitated the viability of keratinocytes in a co-culture system of activated T cells and keratinocytes. Taken together, activated IRGM-autophagy axis under IFN-gamma regulation in T cells might participate in the immunoregulatory mechanism of OLP.

Automated summary

Oral lichen planus (OLP) is an inflammatory immune disease with dense T-cell infiltrate and basal keratinocytes degeneration. The study found that the activated IRGM-autophagy axis in T cells plays a crucial role in OLP patients, and under IFN-gamma regulation, this axis may be involved in the immunoregulatory mechanism of OLP.