الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Rheumatoid arthritis (RA) is a progressive inflammatory autoimmune discase with articular and systemic effects. It affects 1% of the adult population (Choy, 2012). It results from the combination of susceptibility genes and environmental factors (Dieudé, 2009). Most of the identified susceptibility genetic factors are involved in autoimmunity and inflammatory response (Bax et al., 2011). RA patients (> 80%) carry HLA-DRBI *04 epitope and the two alleles of HLA-DRB1 *04 are associated with major organ involvement, nodular disease and surgery related joint destruction (Weyand et al., 1992). In addition to HLA-DR alleles, Genome-wide association studies (GWAS) using single nucleotide polymorphisms (SNPs) have recognized other genes which may be involved in RA susceptibility, mostly genes encoding immune regulatory factors (Kurkó et al., 2013). The SNPs were considered as biomarkers for identifying RA. SNPs variation is more increasing in RA populations than in normal populations. They are found within genes or near genes that are involved in imnunc regulation (Liang and Kelemen, 2011).