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Rheumatoid arthritis (RA) is a systemic and multiple-stage disorder characterized by chronic inflammation with extensive synovitis. The genetic and environmental factors are associated with the risk for RA development.  In RA, the induced IL-16 may play a role in initiating, sustaining and increasing the inflammatory response and development of synovitis, nevertheless IL-16’s actual role in RA pathogenesis must be studied further. This study intended to investigate the association of IL-16 gene polymorphism and RA disease, to determine the genetic role of IL-16 polymorphism and predict the risk of RA development and clinical disease activity. One hundred and Fifty RA patients and 150 apparently healthy control subjects were included in this case-control study. RA disease activity and functional status were evaluated for all RA patients. IL-16 gene polymorphism (SNP rs11556218 T/G) was genotyped using real-time polymerase chain reaction. The difference in IL-16 (rs11556218 T/G) genotype frequencies between RA patients and controls was not statistically significant. However, the G allele was frequently presented in RA patients as compared to controls (p=0.047). Moreover, G allele carriers had two times more risk to develop RA disease than T allele carriers (OR=2.598; 95%CI=1.078-6.825) with dominant genetic association. Alternatively, the G/G genotype was associated with high CDAI, RADAS-5 and HAQ disability index in comparing to other genotypes (T/T-T/G). In conclusion, there was an association between allele G of IL-16 polymorphism (rs11556218 T/G) and risk of RA disease development. In addition, there was an association between genotype G/G and increased clinical disease activity and health disability.

Interleukin 16 polymorphism and susceptibility of rheumatoid arthritis disease in Egyptian population