Altered Autophagy-Associated Genes Expression in T Cells of Oral Lichen Planus Correlated with Clinical Features

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.

Figure 1

Different expression of autophagy-associated genes in T cells of OLP. (a) Heat plot displayed different expression of autophagy-associated genes in peripheral blood T cells from OLP patients and controls. (b) Scatter plot showed expression of autophagy-associated genes, with a fold difference of 2. (c) Volcano plot showed the significant difference in expression of autophagy-associated genes on T cells between OLP patients and control individuals. Fold change and fold regulation bigger than 2 were highlighted in red; fold change less than 0.5 and fold regulation less than −2 were highlighted in green. (d) Multianalysis displayed obvious overexpressed IGF1 mRNA and decreased expression of ATG9B, HGS, ESR1, and SNCA in T cells of OLP.

Figure 2

Expression patterns of autophagy-associated genes in OLP patients and controls based on autophagy array. Expression clusters were indicated by color bars next to the genes and subjects that were included in different clusters. The magnitude of gene expression was present at the bottom of the figure, which represented the gene mRNA relative expression levels by a range of color. Different autophagy-associated genes expression profiles in peripheral blood T cells were shown in two OLP forms and controls (sample 1: nonerosive OLP, NEOLP: sample 2 and sample 3: erosive OLP, EOLP, and control 1, control 2, and control 3: healthy controls).

Figure 3

Expression of IGF1, ATG9B, HGS, ESR1, and SNCA of T cells in OLP patients and controls. (a) Expression of IGF1, ATG9B, HGS, ESR1, and SNCA mRNA in T cells of OLP patients (n = 22) and controls (n = 10). (b–f) The mRNA expression of IGF1, ATG9B, HGS, ESR1, and SNCA in nonerosive OLP patients (NEOLP, n = 11), erosive OLP patients (EOLP, n = 11), and healthy controls (n = 10). Data were shown as mean ± SEM (^∗∗∗ p ≤ 0.001, ^∗ p < 0.05, NS: nonsignificantly).

Figure 4

Expression of IGF1, ATG9B, HGS, ESR1, and SNCA mRNA in T cells from different genders of OLP patients and controls. Data were presented as mean ± SEM (^∗ p < 0.05; NS: nonsignificantly).

Figure 5

Expression of IGF1, ATG9B, HGS, ESR1, and SNCA mRNA in T cells from different age groups of OLP patients. The subjects were divided into three age groups, including those aged < 30 (OLP patients [n = 4] versus controls [n = 3]), those aged 30–50 years old (OLP patients [n = 13] versus controls [n = 4]), and those aged > 50 (OLP patients [n = 5] versus controls [n = 3]). Data were shown as mean ± SEM (^∗ p < 0.05, NS: nonsignificantly).