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Investigating the role of CD24 gene polymorphisms in rheumatoid arthritis
  1. E Sánchez1,
  2. B Fernández-Gutierrez2,
  3. M Á González-Gay3,
  4. A Balsa4,
  5. A García5,
  6. L Rodríguez2,
  7. D Pascual-Salcedo4,
  8. M F González-Escribano6,
  9. J Martin1
  1. 1
    Consejo Superior de Investigaciones Científicas, Granada, Spain
  2. 2
    Servicio de Reumatología, Hospital Clínico San Carlos, Madrid, Spain
  3. 3
    Servicio de Reumatología, Hospital Xeral-Calde, Lugo, Spain
  4. 4
    Servicio de Reumatología e Inmunología, Hospital La Paz, Madrid, Spain
  5. 5
    Servicio de Reumatología, Hospital Virgen del Rocio, Sevilla, Spain
  6. 6
    Servicio de Inmunología, Hospital Virgen del Rocio, Sevilla, Spain
  1. Miss E Sánchez, Consejo Superior de Investigaciones Científicas, Parque Tecnológico de Ciencias de la Salud, Avenida del Conocimiento s/n 18100-Armilla, Granada, Spain; elena{at}ipb.csic.es

https://doi.org/10.1136/ard.2007.084475

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    Rheumatoid arthritis (RA) is a systemic autoimmune disease with a complex pathogenesis which involves genetic and environmental factors.1 CD24 is a glycosylphosphatidylinositol-anchored cell surface protein with expression in a wide variety of cell types which participate in the pathogenesis of RA. This molecule has been proposed as a genetic checkpoint in T-cell homoeostasis and pathogenesis of autoimmune diseases.2 A non-synonymous variation (A57V) and a dinucleotide deletion in the 3′ untranslated region (TG/del) have been associated with different autoimmune diseases, such as multiple sclerosis and systemic lupus erythematosus.3–6 Furthermore, both polymorphisms appear to play a functional role in CD24 expression and CD24 mRNA stability. This gene is located …

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    Footnotes

    • Funding: This work was supported by grant SAF2006-00398 from Plan Nacional de I+D+I, and in part by the Junta de Andalucía, grupo CTS-180.

    • Competing interests: None.

    • Ethics approval: Ethics committee approval was obtained.