The interferon gene signature (IGS) is of increasing interest in patients with autoimmune diseases. In patients with established rheumatoid arthritis (RA), an IGS is present in approximately 20% of patients and associates with poor response to rituximab.1,2 Nevertheless, in patients with established RA, the IGS does not associate with disease activity, and little is known regarding its role in RA pathogenesis.3 However, glucocorticoids, which are commonly administered in patients with RA, can modulate the IGS,2 potentially confounding reported findings.
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Cooles et al. (2017) studied this question.
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