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Rheumatoid arthritis (RA) and juvenile idiopathic arthritis (JIA) are chronic inflammatory diseases that primarily affect the joints. The triggers that activate autoreactive T and B lymphocytes in arthritic patients are still unknown.1 It has been widely assumed, however, that the autoantigens recognised by arthritogenic lymphocytes are joint-specific. This assumption has been challenged by findings from a murine model of spontaneously developing polyarthritis. There, a ubiquitously expressed soluble antigen, the glycolytic enzyme glucose-6-phosphate isomerase (GPI) is the target of autoreactive T cells and arthritogenic antibodies.2
It is, therefore, important to determine if GPI is also relevant to human arthritides. A role for antibodies against GPI in the pathogenesis of RA has been claimed3 and refuted.4–7 Some characteristics of the murine model, such as the lack of rheumatoid factors, resemble JIA rather than RA. Therefore, we tested whether plasma from patients with JIA contained antibodies against GPI. Recombinant human GPI was expressed as described4 and used to test serial dilutions of plasma from patients with JIA or controls matched for age. At a dilution of 1:50, only 1/82 JIA samples and 3/81 controls bound recombinant human GPI (fig 1). Thus, although autoantibodies specific for GPI mediate polyarthritis in a murine model, such antibodies do not occur in a significant fraction of patients with RA or JIA.
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