Tim Family Gene Polymorphism and Susceptibility to Rheumatoid Arthritis: Systematic Review and Meta-Analysis Publisher Pubmed



Razi B¹ ; Reykandeh SE² ; Alizadeh S³ ; Amirzargar A^{2, 4} ; Saghazadeh A^{5, 6} ; Rezaei N^{4, 5, 7}
Source: PLoS ONE Published:2019

Abstract

Background TIM-family proteins are expressed on different immune cells such as dendritic cells, macrophages, type 1 and 2 T helper (Th) cells. Therefore, they have the ability to contribute to the various intracellular signals and immune responses, importantly the regulation of Th1 and Th17 cell differentiation, which plays a remarked role in fight against inflammatory and autoimmune diseases. Association of TIM family gene polymorphisms with rheumatoid arthritis (RA) has been frequently investigated. The findings however are not entirely consistent. Therefore, we carried out the present meta-analysis to examine the association between RA and the following TIM family gene polymorphisms: rs41297579, rs1036199, rs10515746, and rs7700944. Methods A systematic search of Scopus, PubMed, and Web of Science databases was conducted through December 2018. Combined odds ratios (OR) with their corresponding 95% confidence intervals (CI) were calculated under different possible genetic models. Results A total of eight case-control studies were included in the present meta-analysis. The results demonstrated significant association of RA with TIM-3 rs1036199 polymorphism under dominant (OR, 1.93, 95% CI, 1.43–2.61) and allelic models (OR, 1.74, 95% CI, 1.31–2.30). None of the other examined polymorphisms indicated significant association with RA. Conclusions The present meta-analysis revealed that the TIM-3 rs1036199 polymorphism might confer susceptibility to RA. Further studies are required to reassert our findings. © 2019 Razi et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.