Abstract
Oral lichen planus (OLP) is a T cell-mediated inflammatory autoimmune disease. Autophagy has emerged as a fundamental trafficking event in mediating T cell response, which plays crucial roles in innate and adaptive immunity. The present study mainly investigated the mRNA expression of autophagy-associated genes in peripheral blood T cells of OLP patients and evaluated correlations between their expression and the clinical features of OLP. Five differentially expressed autophagy-associated genes were identified by autophagy array. Quantitative real-time RT-PCR results confirmed that IGF1 expression in the peripheral blood T cells of OLP patients was significantly higher than that in controls, especially in female and middle-aged (30–50 years old) OLP patients. In addition, ATG9B mRNA levels were significantly lower in nonerosive OLP patients. However, no significant differences were found in the expression of HGS, ESR1, and SNCA between OLP patients and controls. Taken together, dysregulation of T cell autophagy may be involved in immune response of OLP and may be correlated with clinical patterns.
Highlights
Oral lichen planus (OLP) is a common T cell-mediated chronic inflammatory disease with the characteristics of adult onset, female predilection, and autoimmune attack by infiltrating T cells in the oral mucosa and extraoral lesions on areas including the skin, genitalia, and nails [1, 2]
The results of the autophagy-associated gene expression array used in this study demonstrated an altered expression of autophagy-associated genes in the T cells of OLP patients
The array analysis performed in the present study showed that autophagy related 9 homolog B (ATG9B) expression in T cells was lower in OLP patients
Summary
Oral lichen planus (OLP) is a common T cell-mediated chronic inflammatory disease with the characteristics of adult onset, female predilection, and autoimmune attack by infiltrating T cells in the oral mucosa and extraoral lesions on areas including the skin, genitalia, and nails [1, 2]. OLP mainly manifests three different forms: reticular, atrophic, and erosive [4]. They are generally simplified into two categories: erosive (erosive lesions) and nonerosive (reticular and atrophic lesions) [5]. The immunopathogenesis of OLP may involve antigen presentation, T cell activation and migration, and keratinocyte apoptosis [4]. In OLP, T cells are activated when presented with antigens by major histocompatibility complex (MHC) classes II and I molecules [3, 4]. Following antigen recognition, activated cytotoxic T cells may trigger keratinocyte apoptosis and release chemokines that attract additional helper T cells into the developing OLP lesion. The Th1 immune response plays a dominant role in OLP [4, 6, 7]
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