Rheumatology (Oxford). 2026 Jan 24:keag036. doi: 10.1093/rheumatology/keag036. Online ahead of print.
ABSTRACT
OBJECTIVE: Interferons (IFNs) are implicated in the pathogenesis of rheumatoid arthritis (RA). However, the relationship between serum levels of IFN-α and IFN-γ and the clinical manifestations of RA, particularly regarding cardiovascular comorbidity, remains poorly established. In this study, we aimed to investigate the associations between serum concentrations of IFN-α and IFN-γ and the spectrum of disease manifestations in RA, with special attention to cardiovascular involvement.
METHODS: A total of 216 RA patients were recruited. They underwent comprehensive evaluations, including disease-related characteristics and disease activity indices. Moreover, complete lipid profile, insulin resistance indices, metabolic syndrome criteria, and carotid ultrasound for carotid stiffness, intima-media thickness and carotid plaque detection were assessed. IFN-α and IFN-γ serum levels were measured using Simoa (Single Molecule Array) technique. A multivariable linear regression analysis was performed to examine the associations between the disease characteristics and IFN-α and IFN-γ.
RESULTS: Serum levels of IFN-α and IFN-γ were significantly correlated with each other and were also associated with circulating levels of interleukin 2, 6, and 8. After multivariable adjustment, higher serum IFN-α levels were positively associated with rheumatoid factor and anti-citrullinated protein antibodies positivity, as well as with increased disease activity scores. In contrast, IFN-γ levels showed no significant associations with most clinical manifestations of RA. Furthermore, neither IFN-α nor IFN-γ levels were related to cardiovascular comorbidities, including lipid profiles, insulin resistance indices, or carotid ultrasound findings.
CONCLUSION: Serum levels of IFN-α, but not IFN-γ, are associated with disease activity in patients with RA. However, neither IFN is correlated with the cardiovascular comorbidities commonly observed in this population.
PMID:41578968 | DOI:10.1093/rheumatology/keag036