Investigation of association between toll-like receptor polymorphisms and autoantibody pozitive

Rheumatoid arthritis (RA) which is a chronic, inflammatory disease affecting primarily the joints influences cognitive functions negatively, although the underlying mechanisms have not been clarified yet. There is an important role of antigen-presenting cells (APCs) such as macrophages and dendritic cells (DCs) in RA etiology. These cells have some receptors known as Toll Like receptor (TLR), responsible doğal and adaptive immune response. This study is conducted to investigate TLR3, TLR4, TLR9 and TLR10 polymorphism freguency and to detect between polymorphisms and autoantibody positive as RF, kollajen tip II, anti-RNP ve anti-CCP in patient group.In this study, 100 RA subjects according to the American College of Rheumatology remission criteria (ACR), ranging with varying degrees of disease activity and a control group of 100 healthy subjects matched by age and sex, without any joint diseases were evaluated. DNA izolation was performed from using conventional methods from peripheral blood samples of RA and control group. The detection of all polymorphisms was used Restriction Fragment Lenght Polymorphism (RFLP) method. In this study was evaluated TLR3 rs3775290, TLR4 rs4986790 and rs4986791, TLR9 rs187084 and TLR10 rs4129009 polymorphisms. Serum autoantibody level was measured using quantitative ELISA.There was statistically significant differences between patients and control groups with regard to TLR4 gene Asp299Gly (p=0.02) and Thr399Ile allel freguencies (p=0.05). We detected the increased freguency for two allel in patients group. Statistically significant difference for TLR9 genotype between patients and control group was seen. TLR9 C allele was found to be a protective factor against developing RA. It was found no statistically significant differences in the TLR3 and the TLR10 genotype or allele distribution between RA patients and control individuals.Tissue damage resulted inflammation may be a cause of chronic inflammation in RA the released proinflamatory cytokine by TLR with feed back mechanism. We consider that the increased TLR4 mutant allel and the decreased TLR9 C allele was associated with a higher risk of RA. Further studies are required to explore the role of TLR gene polymorphisms in the risk of RA, especially in ethnically different populations to confirm our results.