Document Type : Original Article

Authors

1 Department of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

2 Rheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran. Inflammation Research Center, Tehran University of Medical Sciences, Tehran, Iran.

3 Rheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran.

4 Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

Abstract

The critical role of IFN signature genes has increasingly been surveyed to determine the etiology and pathogenesis of systemic
sclerosis (SSc). Interferon-regulatory factors (IRFs) and signal transducers and activators of transcription (STATs) are mainly
considered as transcriptional modulators of IFN-signature genes and type I interferon and play a major role in the regulation of
numerous aspects of an immune response. The current study aimed to assess the transcriptional levels of IRF7 (interferonregulatory factor 7) and STAT1 (signal transducers and activators of transcription 1) mRNAs in PBMCs of scleroderma patients
and compare them with those of healthy subjects.
In this study, PBMCs were obtained from 50 scleroderma patients and 30 healthy individuals. Subsequently, total RNA was
extracted from isolated PBMCs and cDNA synthesis was carried out. IRF7 and STAT1 mRNA expressions were assessed by
applying quantitative real-time PCR, SYBR Green method, and specific primers for IRF7 and STAT1.
Relative expression of IRF7 was significantly increased in the patient group compared with the control group. Moreover, relative
expression of IRF7 in limited SSc (lSSc) and diffuse SSc (dSSc) was significantly increased compared with healthy subjects (
p
< 0.05). The relative expression of STAT1 transcripts in PBMCs was not statistically significantly different between the patient
group and the control group. The correlation between IRF7 expression and the Rodnan score (RS) of the disease was significant.
Considering the overexpression of IRF7 in SSc patients and significant correlation between the IRF7 and the Rodnan score of
the disease, it is suggested that impaired expression of IRF7 is involved in the pathogenesis of SSc.

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