TNF-α, TNF-β and IL-10 gene polymorphism and association with oral lichen planus risk in Saudi patients

Abstract

Objectives Oral lichen planus (OLP) is a chronic inflammatory oral mucosal disease. Cytokines play an important role in the pathogenesis and disease progression of OLP. Various reports have implicated cytokine gene polymorphisms in susceptibility to develop some immune mediated conditions including OLP. The purpose of this study was to investigate the association of tumor necrosis factor (TNF)-α, TNF-β and interleukin (IL)-10 gene polymorphisms with the OLP risk.Material and Methods Forty two unrelated patients with OLP and 211 healthy volunteers were genotyped for TNF-α (-308 G/A), TNF-β (+252A/G), IL-10 (-1082G/A), IL-10 (-819C/T), and IL-10 (-592C/A) polymorphisms.Results The frequencies of allele A and genotype GA of TNF-α (-308G/A) were significantly higher while allele G and GG genotypes were lower in OLP patients as compared to the controls (P<0.001). The frequency of GA genotype of TNF-β (+252A/G) was significantly higher in patients than in controls while the AA genotype was completely absent in OLP patients. These results indicated that allele A and genotype GA of TNF-α (-308G/A) as well as the GA genotype of TNF-β (+252A/G) polymorphisms are associated with OLP risk. The frequencies of alleles and genotypes of -1082G/A, -819C/T and -592C/A polymorphisms in IL-10 gene did not differ significantly between OLP patients and controls (P>0.05). However, haplotype ATA extracted from 1082G/A, -819C/T, -592C/A polymorphisms of IL-10 were more prevalent in OLP patients when compared to controls indicating its possible association with OLP susceptibility.Conclusion It is concluded that TNF-α (-308G/A), TNF-β (+252A/G) and IL-10 (-1082G/A, -819C/T and -592C/A) polymorphisms are associated with the susceptibility of OLP, thus giving additional support for the genetic basis of this disease.

Association between polymorphisms in interleukins and oral lichen planus

“…The total number of studies related to the SNP of ILs is shown in Table S2. Eventually, 6 studies [18–20,24–26] including 4 SNPs (IL6-174G/C, IL10-592C/A, IL10-819C/T, and IL10-1082G/A) meeting the inclusion criteria were included for the ultimate quantitative analysis. All of the SNPs of ILs which were not analyzed in this meta-analysis were concluded in qualitatively in Table S2.…”

“…Of these included studies, a total of 362 OLP patients and 622 non-OLP control subjects from 5 different countries were covered. Three of 6 studies [18,25,26] focused on the SNP of IL6-174G/C, whereas 4 of 6 studies [19,20,24–26] focused on IL10-592C/A, IL10-819C/T, and IL10-1082G/A, respectively. The characteristics of the included studies, including the P value for HWE and quality assessment are summarized in Table 1 and S3.…”

“…[15,16] More and more studies suggested that SNPs in interleukins genes, such as IL4 (−590T/C, −1098T/G), IL6 (−174G/C), IL10 (−592C/A, −819C/T, and −1082G/A), and IL18 (−137G/C, −607C/A), were correlated with development OLP or the severity of OLP. [17–20] However, these results were mixed, inconclusive, and even inconsistent. Despite that Lu et al [9] have briefly reviewed some of the research results on gene polymorphisms of several ILs in patients with OLP, specialized studies to quantitatively assess the presence and strength of the association between OLP and polymorphism of several ILs are still lacking.…”

Clinical characteristics and analysis of familial oral lichen planus in eight Chinese families

“…Previously, OLP has been reported to be associated with systemic medical conditions, such as diabetes, hepatitis C viral infections, hypertension, ulcerative colitis, myasthenia gravis and lupus erythematosus (2,3,4,11). Recently, several studies have revealed the genetic susceptibility of OLP through case control association testing (14)(15)(16)(17).…”

Inflammatory Bowel Disease: The Association of Inflammatory Cytokine Gene Polymorphisms

“…TNF-α (-308) promoter polymorphism leads to a less common allele-A (allele 2), which has been associated with increased TNF-α production in vitro [33,34] and higher rate of TNF-α transcription than wild-type GG genotype [35,36]. This polymorphism has been linked to increased susceptibility to several chronic metabolic degenerative, inflammatory and autoimmune diseases [37][38][39][40][41].…”