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Declined hTERT expression of peripheral blood CD 4 + T cells in oral lichen planus correlated with clinical parameter
Author(s) -
Zhang Jing,
Wei Minghui,
Lu Rui,
Du Gefei,
Zhou Gang
Publication year - 2016
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/jop.12399
Subject(s) - telomerase reverse transcriptase , telomerase , oral lichen planus , t cell , immunology , immune system , telomere , protein subunit , peripheral blood mononuclear cell , biology , microbiology and biotechnology , cancer research , medicine , in vitro , gene , biochemistry
Background Oral lichen planus ( OLP ) is a chronic, T‐cell‐mediated inflammatory autoimmune disease. Human telomerase reverse transcriptase ( hTERT ), a catalytic subunit bearing the enzymatic activity of telomerase, may have a unique function in regulating the activation, proliferation, and function of T lymphocytes. The goal of this study was to investigate the expression of hTERT in CD 4 + and CD 8 + T cells from patients with OLP and its correlation with clinical parameter. Methods The disease severity of OLP was assessed by RAE (reticular, atrophic, erosive) scoring system. Expressions of hTERT in CD 4 + T cells and CD 8 + T cells isolated from peripheral blood of patients with OLP were detected by real‐time PCR , and their correlations with clinical features were analyzed. Results hTERT mRNA levels in CD 4 + T cells of OLP were significantly lower than that of controls, while the levels in CD 8 + T cells showed no statistical difference. The expression of hTERT in CD 4 + T cells and CD 8 + T cells was neither associated with disease severity nor gender. CD 4 + T cells of OLP patients with the age ≤50 had markedly decreased hTERT levels compared with controls, but CD 8 + T cells did not. Conclusions A divergent hTERT pattern between CD 4 + and CD 8 + T cells was implicated in OLP . Decreased hTERT in CD 4 + T cells might be responsible for the immune dysfunction in OLP.