The expression of interferon-stimulated genes (interferon “signature”) in patients with rheumatoid arthritis (Preliminary results)

• Published in: Nauchno-prakticheskai͡a︡ revmatologii͡a Vol. 58; no. 6; pp. 673 - 677
• Main Authors: Avdeeva, A. S., Tchetina, E. V., Cherkasova, M. V., Markova, G. A., Artyuhov, A. S., Dashinimaev, E. B., Nasonov, E. L.
• Format: Journal Article
• Language: English
• Published: IMA PRESS LLC 14.01.2021
• Subjects: interferon signature; interferon-stimulated genes; rheumatoid arthritis
• ISSN: 1995-4484; 1995-4492
• DOI: 10.47360/1995-4484-2020-673-677

Objective. To assess the expression of interferon-stimulated genes in patients with rheumatoid arthritis (RA).Material and methods. Twenty patients with RA were examined. All patients received methotrexate therapy at a stable dose (Me 15 [10-17.5] mg) for at least 4 weeks. To assess the Type I IFN gene signature (IFNGS) we selected five genes (IFI44L, MX1, IFIT1, RSAD2, EPSTI1). The expression of IFI44L and IFIT1 could not be determined, and further analysis took into account three genes - MX1, EPSTI1, RSAD2.Results. Baseline level of MX1 expression - 11.48 [5.45-19.38], EPSTI1 - 12.83 [5.62-19.64], RSAD2 - 5.16 [2.7310.4] and IFN score - 10.3 [5.18-17.12] in patients with rheumatoid arthritis was significantly higher compared with healthy donors - 1.26 [0.73-1.6], 1.06 [0.81-1.48], 0.93 [0.72-1.19], and 1.09 [0.92-1.42] respectively, p<0.05. IFN signature was found in 15 (75%) patients, was absent - in 5 (15%) patients. A positive correlation was found between the IFNGS and the level of EPSTI1 expression with the duration of methotrexate therapy (r=0.46, p=0.03). Among patients who received methotrexate therapy for more than one year, there was a tendency to a higher level of EPSTI1 expression (10.74 [12.6-32.8]) and IFNGS (16.2 [8.9-38.3]) compared with patients taking methotrexate for less than a year (9.67 [5.4-14.2] and 7.9 [4.5-13.4]), (p=0.06).Conclusion. Preliminary results on the assessment of IFNGS indicate an increased expression of IFN-stimulated genes in patients with RA, which may be important for predicting the course of the disease and personalizing therapy.