Response to: 'Circulating interferon-α measured with a highly sensitive assay as a biomarker for juvenile inflammatory myositis activity.' by Melki et al
Résumé
We thank Dr. Melki and colleagues for their interest in our work on IFNα assessment in SLE. In their correspondence, they show that IFNα protein measurement by digital ELISA is also correlated with disease activity in other IFN-dependent autoimmune diseases, and in this case, juvenile IIMs. Since IFNs (especially IFNα) are involved in the pathogenesis of several autoimmune diseases such as SLE, myositis, Sjögren's syndrome, and systemic sclerosis (1), monitoring their presence in the circulation of patients might help physicians to better evaluate disease activity and/or predict future flares. However, until recently, clinicians lacked a robust and standardized method for the measurement of IFNs in serum because IFN concentrations are usually very low and often not detectable with the use of classic immunoassays. Tools for indirect measurement of IFNα activity through an IFN gene expression score have a very low availability. These scores are not only notoriously difficult to standardize but are also less sensitive to change than direct measurement of IFNα. The advent of the ultrasensitive Simoa digital ELISA technology now makes it possible to reliably measure very low concentrations of IFNα (2). The studies by Melki et al and ourselves show that direct measurement of IFNα might improve monitoring of clinical activity in myositis and SLE, respectively. Of note, the area under the ROC curve value of 0.81 for IFNαconcentration as a discriminator between active versus inactive juvenile IIM determined by Melki and colleagues is similar to the value of 0.83 that we had previously reported in SLE. In Melki and colleagues' study, the optimal cutoff threshold of IFNαconcentration permitting the ability to distinguish active from inactive juvenile IIM was 42 fg/ml,
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