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Declined hTERT expression of peripheral blood CD4+ T cells in oral lichen planus correlated with clinical parameter

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...

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Bibliographic Details
Published in:Journal of oral pathology & medicine 2016-08, Vol.45 (7), p.516-522
Main Authors: Zhang, Jing, Wei, Ming-hui, Lu, Rui, Du, Ge-fei, Zhou, Gang
Format: Article
Language:English
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Summary: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 CD4+ and CD8+ 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 CD4+ T cells and CD8+ 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 CD4+ T cells of OLP were significantly lower than that of controls, while the levels in CD8+ T cells showed no statistical difference. The expression of hTERT in CD4+ T cells and CD8+ T cells was neither associated with disease severity nor gender. CD4+ T cells of OLP patients with the age ≤50 had markedly decreased hTERT levels compared with controls, but CD8+ T cells did not. Conclusions A divergent hTERT pattern between CD4+ and CD8+ T cells was implicated in OLP. Decreased hTERT in CD4+ T cells might be responsible for the immune dysfunction in OLP.
ISSN:0904-2512
1600-0714
DOI:10.1111/jop.12399