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Ankylosing spondylitis (AS) is a common chronic rheumatic disease whose aetiology arises as a result of the contribution of environmental factors and a strong genetic component.1 One crucial point in the pathogenesis of the disease is the regulation of T cell response.2 Recently, it has been shown that the functional 1858 C/T polymorphism of PTPN22, the gene that encodes a lymphoid-specific protein tyrosine phosphatase (LYP), is associated with several autoimmune diseases (ADs), supporting the hypothesis that common aetiopathological pathways are shared by different ADs.3 LYP has a key role as a negative regulator of T cell activation.4 It seems that the single nucleotide polymorphism (SNP) 1858 C/T disrupts the interaction …
Conflict of interest: None.
Published Online First 8 September 2005
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