Interferon-induced protein 44 (IFI44) and interferon regulatory factor 4 (IRF4) gene expression in rheumatoid arthritis.

Abstract

Background and objectives: The type I interferon (IFN) signature has been found to be overactivated in many systemic autoimmune diseases. This may be explained by impaired regulation of interferon-stimulated genes (ISGs) as well as interferon-induced protein 44 (IFI44) expression via their regulatory mechanisms via interferon regulatory factors (IRFs).

Patients and methods: This case-control study includes two groups: 50 RA patients and 50 healthy controls. The quantification of IFI44 and IRF4 expression levels by the real-time PCR technique was estimated. Disease Activity Score-28 (DAS-28) was estimated for RA patients only.

Results: Among the RA patients, there were statistically significant increased ESR, CRP, TLC, RF, and anti-CCP levels (p value < 0.001) and significant increased expression of the IFI44 and IRF4 genes (p value < 0.001). There was a significant positive correlation between the IFI44 and IRF4, and there was a significant correlation between both and ESR and anti-CCP among RA patients. At a cutoff point of 1.95, IFI44 shows higher sensitivity and specificity values than IRF4 for the diagnosis of RA.

Conclusion: IFI44 was more sensitive for RA diagnosis than IRF4. IFI44 and IRF4 overexpression could be promising predictors of RA diagnosis and might become useful clinical tools to guide therapeutic strategies.