Investigation of the Relationship of IL-17 Gene Variants with Rheumatic Heart Disease

INTRODUCTION: Rheumatic heart disease (RHD) results from rheumatic fever (RA) caused by streptococcal throat infection. 3-6% of patients with rheumatic fever turn into RHD. Recent studies have shown that Th17 cells, a newly identified new effector T cell line, play a role in the pathogenesis of RHD. Host auto-reactivity mediated by cellular and humoral immune responses is known to play a role in RHD development, and interleukin (IL)-17 appears to be the leading actors in this process. Despite this central role in RHD pathogenesis, the number of studies on IL-17 variants is very limited. Moreover, there is no data related to this issue in Turkish society. Therefore, in this study, we aimed to investigate the relationship between IL-17A rs2275913 and IL-17F rs763780 polymorphisms in the pathogenesis of RHD. METHODS: In this case-control study, the study group consisting of 390 women (170RHD/220 control) IL-17A rs2275913, IL-17F rs763780 gene variants were examined using the TaqMan 5 'Allelic Discrimination Test method. RESULTS: The IL-17A rs2275913 genotype distributions among study groups were statistically significant (p=0.010). In addition, the IL-17A rs2275913 AA genotype was found in both single valve lesions (p=0.021) and combined valve lesions (p=0.038). It was statistically higher compared to the group. IL-17F rs763780 variants showed no association with RHD pathogenesis. DISCUSSION AND CONCLUSION: Based on our findings, we would like to report that the IL-17A rs2275913 variant is effective in both the pathogenesis and severity of RHD, and that we found a serious correlation in defining high sensitivity. We think that IL-17A rs2275913 variants can be recommended as a suitable biomarker for the identification of susceptible individuals in the Turkish population.