Association of polymorphisms in Th1/Th2-related cytokines (IFN-γ, TGFβ1, IL-1β, IL-2, IL-4, IL-18) with oral lichen planus: A pooled analysis of case-control studies

J Dent Sci. 2023 Apr;18(2):560-566. doi: 10.1016/j.jds.2022.08.032. Epub 2022 Sep 16.

Abstract

Background/purpose: Increasing evidence suggests that single-nucleotide polymorphisms (SNPs) in Th1/Th2-related cytokine genes correlated with oral lichen planus (OLP) susceptibility. However, these results were inconsistent and inconclusive. Hence, the aim of this study is to draw a more precise estimation of the genetic associations between SNPs in 6 cytokines (IFN-γ, IL-18, TGFβ1, IL-1β, IL-2, IL-4) and OLP.

Materials and methods: A systematic literature search was conducted to identify all eligible case-control studies on the association between SNPs in 6 cytokines and OLP susceptibility. Odds ratios (ORs) and 95% confidence intervals (CIs) from each study were pooled to estimate the strength of the association.

Results: A significant association of IFN-γ (874A/T) polymorphism with OLP was found (OR, 1.49; 95%CI, 1.22-1.81; P < 0.001) based on 6 eligible studies. A significant association of IL-18 (137G/C) polymorphism with OLP was found (OR, 1.64; 95%CI, 1.24-2.18; P < 0.001) based on 3 studies. A marginally significant association of TGFβ1 (509C/T) polymorphism in allele model with OLP was found (OR, 1.31; 95%CI, 1.01-1.71; P = 0.05) based on 4 studies. Nevertheless, lack of significant association of IL-1β (3954C/T), IL-2 (330T/G), IL-4 (590C/T), and IL-18 (607C/A) polymorphisms with OLP was found (P > 0.05) based on 3 studies, respectively.

Conclusion: This is the first meta-analysis to investigate the associations of 6 cytokines polymorphisms with OLP, suggesting that SNPs in IFN-γ, IL-18, and TGFβ1 may act as genetic factors for OLP risk. Further well-designed studies with larger sample size and multiple ethnicities are needed to validate these associations.

Keywords: Cytokines; Meta-analysis; Oral lichen planus; Single-nucleotide polymorphisms; T helper cells.