Journal
ARTHRITIS RESEARCH & THERAPY
Volume 23, Issue 1, Pages -Publisher
BMC
DOI: 10.1186/s13075-021-02414-0
Keywords
Systemic lupus erythematosus; Interferon; Disease course; SLEDAI-2K
Categories
Funding
- Canadian Institutes of Health Research (CIHR-QNT) [78341]
- Canada Research Chair on systemic autoimmune rheumatic diseases at Universite Laval
- Arthritis Society Young Investigator Award
- Canadian Rheumatology Association (CIORA) -Arthritis Society Clinician Investigator Award
- Arthritis Centre of Excellence of the University of Toronto
- Department of Medicine Merit Award
- Pfizer Chair Career Award
- tenured Professorship of Medicine at Universite Laval
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By measuring the levels of interferon-responsive genes, the course of disease activity and treatment outcomes in SLE patients over the next 5 years can be predicted. A high baseline IFN5 level is associated with more severe outcomes.
Objectives: Type I interferons (IFNs) play an important role in the pathophysiology of systemic lupus erythematosus (SLE). While cross-sectional data suggest an association between IFN-induced gene expression and SLE disease activity, interest in this as a biomarker of flare has been tempered by a lack of fluctuation with disease activity in the majority of patients. This led us to question whether IFN-induced gene expression might instead be a biomarker of overall disease severity, with patients with high levels spending more time in an active disease state. Methods: Levels of five interferon-responsive genes were measured in the whole peripheral blood at baseline visit for 137 SLE patients subsequently followed for 5 years. Log transformed values were summed to yield a composite IFN5 score, and the correlation with various disease outcomes examined. Receiver operator characteristic analyses were performed for outcomes of interest. Kaplan-Meier curves were generated to compare the proportion of flare-free patients with high and low IFN5 scores over time. Results: The baseline IFN5 score was positively correlated with the adjusted mean SLE disease activity index-2000, number of flares, adjusted mean prednisone dose, and number of new immunosuppressive medications over the subsequent 5 years. Optimal cut-offs for the IFN5 score were determined using Youden's index and predicted more severe outcomes with 57-67% accuracy. A high baseline IFN5 level was associated with a significantly increased risk of subsequent flare. Conclusions: Measurement of the type I IFN signature is a useful tool for predicting the subsequent disease activity course.
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