الفهرس | Only 14 pages are availabe for public view |
Abstract Rheumatoid arthritis is an inflammatory autoimmune disease affecting humans throughout the world causing joint inflammation, swelling and pain. Wide variety of factors together with environmental and genetic elements contribute to the disease pathogenesis and progression. Genome scanning indicated a strong genetic component, revealing that there is more than one region that is linked to disease. There is a great deal of evidence that points to the contribution of TNF-α and β gene as a common genetic factor in the pathogenesis of diseases caused by inflammatory and/or autoimmune aetiologies. Production of TNF α and β is thought to be controlled by genetic polymorphisms in the genes regulating their production and effect. Also, single nucleotide polymorphisms (SNPs)in the TNFα and β genes themselves have functional significant role in the regulation of their production as there are many SNPs within the TNFα and β gene promoter. Genetically controlled production of TNFα and β lead to differences in their synthesis; which in turn could imply influence of TNFα and β polymorphism on RA susceptibility or severity. This study focuses on 4SNPs in TNF α gene (238,308,857,863), 1SNPin TNF β gene (252) and their association with RA activity (using DAS28ESR score). |