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

Mediators Inflamm. 2016:2016:4867368. doi: 10.1155/2016/4867368. Epub 2016 Feb 15.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Endosomal Sorting Complexes Required for Transport / metabolism
  • Estrogen Receptor alpha / metabolism
  • Female
  • Gene Expression Regulation / genetics
  • Gene Expression Regulation / physiology
  • Humans
  • Lichen Planus, Oral / genetics
  • Lichen Planus, Oral / metabolism*
  • Lichen Planus, Oral / pathology*
  • Male
  • Middle Aged
  • Phosphoproteins / metabolism
  • T-Lymphocytes / metabolism*
  • Young Adult
  • alpha-Synuclein / metabolism

Substances

  • ESR1 protein, human
  • Endosomal Sorting Complexes Required for Transport
  • Estrogen Receptor alpha
  • Phosphoproteins
  • SNCA protein, human
  • alpha-Synuclein
  • hepatocyte growth factor-regulated tyrosine kinase substrate