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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 …
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.
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