Abstract

The upregulation of IFN pathways and their stimulated genes is associated with primary Sjögren’s syndrome (pSS). The recent studies also indicate the involvement of interferon γ (IFNγ) in the pathogenesis of pSS. The study aimed to assess the clinical and immunological activity depending on the concentration of IFNγ in the peripheral blood in pSS patients. Methods: The study group consisted of patients over 18 years of age with a confirmed diagnosis of pSS. Based on the collected data, disease activity was assessed using the EULAR Sjögren’s syndrome disease activity index (ESSDAI) and the EULAR Sjögren’s syndrome patient reported index (ESSPRI). Results: Among 40 pSS patients, 33 (82%) showed increased levels of IFNγ. The group with positive IFNγ was younger (43 years) than the group with negative IFNγ (57 years) (p < 0.05). In the positive IFNγ group, the time to diagnosis was shorter (p < 0.05). There was a difference in ESSDAI among patients with and without IFNγ (p < 0.05). There were no differences between the groups in ESSPRI and the presence of cryoglobulins, specific anti-SSA, and anti-SSB antibodies and in C3 and C4 hypocomplementemia. RF occurred in both groups with a similar frequency (p = 0.6), but in patients with IFNγ presence, significantly higher RF titers were observed (34.9 vs. 10.5; p < 0.05). Conclusion: In the group of patients with positive IFNγ, the mean value of RF and ESSDAI was higher. This group was also younger than patients with pSS without IFNγ.

Highlights

  • Publisher’s Note: MDPI stays neutralSjögren’s syndrome (SS) is the second most common autoimmune disorder after rheumatoid arthritis (RA) [1]

  • In the EULAR Sjögren’s syndrome patient reported index (ESSPRI) questionnaire, greater severity of the reported dryness symptoms was found in the interferon γ (IFNγ) negative group than in the positive group (6.1 vs. 4.6)

  • We present the relationship between the serum concentration of IFNγ in patients with diagnosed Primary SS (pSS) and the clinical course and immune picture of the disease

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Summary

Introduction

Sjögren’s syndrome (SS) is the second most common autoimmune disorder after rheumatoid arthritis (RA) [1]. Primary SS (pSS) is considered a multifactorial disease, where a susceptible genetic background requires an environmental factor trigger, such as viral infection [2], to initiate the development of the disease. Many genes, including IRF5, STAT4, and IL12A, regulate the interferon (IFN) system [3,4]. The upregulation of IFN pathways and their stimulated genes are associated with the clinical symptoms of SS [5,6]. There are three main groups of IFN: type I, which includes various forms of IFNα and one IFNβ; type II IFN charge IFNγ; and type III IFN-λ consisting of IL-29, IL-28A, and IL-28B. The studies conducted so far among patients with pSS indicate that IFN may play a significant role in the pathogenic mechanism and development of clinical symptoms

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