Protein tyrosine phosphatase-22 (PTPN-22) polymorphism in the pathogenesis of chronic urticaria.

摘要

Pathophysiology of chronic urticaria (CU) includes inflammatory, hormonal as well as autoimmune abnormalities. Autologous serum skin test (ASST) is a valuable marker of circulating functional autoantibodies. From the clinical point of view, the coexistence of CU and autoimmunity has been well documented. The genetic basis of autoimmune disorders is gradually uncovered. Protein tyrosine phospha-tase-22 (PTPN-22) is located at Ip13.3-p1 3.1 and is considered to be the strongest genetic factor for human autoimmunity besides MHC (1). Polymorphism in the PTPN-22 (1858C>T) is associated with the risk of development of multiple autoimmune diseases such as systemic lupus erythematosus (SLE), rheumatoid arthritis and type 1 diabetes (2). Additionally, it was proved to be associated with Graves' Disease and Hashimoto's thyroiditis (3, 4). 1858C>T causes a functional change in lymphoid tyrosine phosphatase protein (Lyp). Disease-associated T allele encodes a protein not binding to the protein tyrosine kinase Csk, which results in hyperresponsiveness of T cells. Generally, 1858C>T variant is associated with these autoimmune disorders that present contribution to autoantibodies. Because several forms of autoimmunity have been associated with CU, we decided to evaluate whether PTPN-22 T allele is associated with CU in the Polish population.