The Association of Genetic Polymorphisms in Tumor Necrosis Factor-Alpha and Interleukins with Disease Severity or Response to Biological Therapy in Iraqi Rheumatoid Arthritis Patients: A Narrative Review

Abstract

Background: Tumor necrosis factor-alpha (TNF-α) and interleukins play important roles in the pathogenesis of rheumatoid arthritis (RA). Genetic research has been employed to find many of the missing connections between genetic risk variations and causal genetic components. Objective: The goal of this study is to look at the genetic variations of TNF-α and interleukins in Iraqi RA patients and see how they relate to disease severity or response to biological therapy. Method: Using specific keywords, the authors conducted a systematic and comprehensive search to identify relevant Iraqi studies examining the genetic variations of TNF-α and interleukins in Iraqi RA patients and how they relate to disease severity or response to biological therapy. Results: Thirteen studies have looked at TNF-α and interleukin genetic polymorphisms in Iraqi RA patients. Only the IL-2, IL-4, IL-6, IL-17, and IL-23 receptor gene polymorphisms were explored for interleukins; however, the results of studies indicate no association between genetic polymorphism and the severity of RA. Very few researchers examine the correlation between genetic variation and TNF-α inhibitor responsiveness. Numerous studies have been conducted to investigate the genetic variations of the TNF-α promoter. The -308 G/A region in the promotor region was the most studied location.