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Abstract

The objective review is to inspect the involvement of Interleukin-6 (IL-6) in rheumatoid arthritis (RA) and to highlight the role of IL-6 and its variants in the pathogenesis of RA and response to anti-IL-6 agents. Several genetic and environmental risk factors and infectious agents contributed to the development of RA. Interleukin-6 is engaged in self-targeted immunity by modifying the equilibrium between T regulatory (T-_reg) and T helper-17 (T_h-17) cells. The evidences reported that IL-6 participated in RA pathogenies including synovitis, angiogenesis, joint damage, and dislocations of bone. IL-6 induces peripheral and central pain sensitization that provokes chronic pain development. Many IL-6 loci contribute to the risk of RA development. Several IL-6 gene variants were studied, which included; -174, -572, -597, and -622 in the 5-flanking region (Promotor). The current data demonstrates the significant role of IL-6 promoter Single Nucleotide Polymorphisms (SNPs), particularly G (-174) C, in the susceptibility and pathogenesis of RA. The C allele linked with the risk, the genotypic and allelic frequencies were higher in Asian and Indian RA patients. Elevated serum IL-6 levels are observed in mutant homozygote CC carriers at the -174 locus, which could explain the impact of this SNP on RA. It seems that age, ethnicity, geographic region, and lifestyle impact the effect of the IL-6 variant in RA. In conclusion; because IL-6 plays a central role in the pathogenesis of RA and its symptoms, it can be speculated that IL-6 promoter SNP (rs1800795) could be a risk agent for RA‎.

Keywords: Rheumatoid arthritis, Interleukin-6, Genetics, Polymorphism, Pharmacogenetics

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