الفهرس 
Rheumatoid arthritis
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Abstract
Rheumatoid arthritis (RA) is a synovial inflammatory disease of unknown etiology that occurs in about 1% of the population. The onset is typically between ages 30 and 55 years with women nearly twice as likely to develop the disease. It is characterized by the chronic inflammation and destruction of the synovial joints leading to progressive joint damage and disability. Although the etiology of RA is unknown, both genetic and environmental factors have been shown to play a role in its development. Genetic factors were thought to be responsible for up 50–60% of the predisposition to RA. The genetic background of RA is complex and likely involves many genes which encode proteins with significant functions in the regulation of immune response. The protein tyrosine phosphatase non-receptor type 22 (PTPN22) gene, is located on chromosome 1p13, and encodes a lymphoid specific phosphatase (LYP), which is important in negative control of T cell activation and in T cell development. PTPN22 gene belongs to a family of protein tyrosine phosphatase involved in preventing spontaneous T cell activation by dephosphorylation and inactivation of T cell receptor-associated kinases. The PTPN22 +1858 C>T SNP changes the amino acid at position 620 from an arginine (R) to a tryptophan (W) and disrupts the interaction between Lyp and Csk and thus inhibits complex formation and suppresses Tcell activation.