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Lack of association between ankylosing spondylitis and a functional polymorphism of PTPN22 proposed as a general susceptibility marker for autoimmunity
  1. G Orozco1,
  2. C García-Porrúa2,
  3. M Á López-Nevot3,
  4. E Raya4,
  5. M Á González-Gay2,
  6. J Martín1
  1. 1Instituto de Parasitología y Biomedicina López Neyra, Granada, Spain
  2. 2Sección de Reumatología, Hospital Xeral-Calde, Lugo, Spain
  3. 3Servicio de Inmunología, Hospital Virgen de las Nieves, Granada, Spain
  4. 4Servicio de Reumatología, Hospital Clínico San Cecilio, Granada, Spain
  1. Correspondence to:
    Dr J Martín
    Instituto de Parasitología y Biomedicina López Neyra, CSIC, Parque Tecnológico de Ciencias de la Salud, Avenida del Conocimiento s/n 18100-Armilla, Granada, Spain; martin{at}ipb.csic.es

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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 …

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