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Published on: April 1, 2019
TLR2, TLR4 and CD86 gene polymorphisms in recurrent aphthous stomatitis
Jumana Karasneh1, Maisoun Bani-Hani2, Asem Alkhateeb2
1Department of Oral Medicine and Oral Surgery, Jordan University of Science and Technology (JUST), Irbid, Jordan.
Genetic variations in Toll-like receptor 4 (TLR4) may increase the risk of recurrent aphthous stomatitis (RAS). This study found a significant association between a specific TLR4 gene polymorphism (rs10759931) and RAS, suggesting a potential role for TLR4 in the disease.
Area of Science:
- Immunology
- Genetics
- Oral Medicine
Background:
- Recurrent aphthous stomatitis (RAS) is an inflammatory condition influenced by genetic and environmental factors.
- Toll-like receptors (TLRs) and CD86 are crucial for innate immunity and cellular immune responses.
- Investigating genetic polymorphisms in TLRs and CD86 may reveal associations with RAS susceptibility.
Purpose of the Study:
- To determine if specific polymorphisms in the Toll-like receptor 2 (TLR2), Toll-like receptor 4 (TLR4), and CD86 genes are associated with recurrent aphthous stomatitis (RAS).
Main Methods:
- Genotyping of eight single nucleotide polymorphisms (SNPs) in TLR2, TLR4, and CD86 genes using PCR-RFLP in 96 RAS patients and 153 controls.
- Association analysis performed using logistic regression.
- Linkage disequilibrium assessed with Haploview software.
Main Results:
- A significant association was observed between the TLR4 rs10759931 polymorphism (A allele and AA genotype) and an increased risk of RAS.
- Increased inheritance of the TLR4 rs1927911 C allele and CC genotype showed a trend towards association with RAS, but did not reach statistical significance.
- No significant association was found between TLR2 or CD86 gene polymorphisms and RAS.
Conclusions:
- This study is the first to explore the link between TLR and CD86 gene polymorphisms and RAS.
- The TLR4 rs10759931 polymorphism is significantly associated with recurrent aphthous stomatitis.
- Further research, including studies in diverse populations and functional analyses, is warranted to elucidate the role of TLR4 in RAS pathogenesis.
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