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The Level of TGF-β in Sera of Patients with Primary Sjögren's Syndrome

Overview
Journal Reumatologia
Publisher Termedia
Specialty Rheumatology
Date 2020 Apr 1
PMID 32226163
Citations 4
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Abstract

Objectives: Tumor growth factor β (TGF-β) is a pleiotropic cytokine which controls autoimmune reactions, cell proliferation, and the organ accumulation of lymphocytes. This cytokine has a protective and anti-inflammatory effect in autoimmune processes, but also has a pro-fibrinous activity. Therefore, its importance in the development of systemic sclerosis has been proven. The role of TGF-β in Sjögren's syndrome is also a valid direction of research. The aim of the presented study is to evaluate the level of TGF-β in sera of primary Sjögren's syndrome patients and to investigate possible correlations with autoantibodies, cytokines, and cells in biopsy of minor salivary glands active in the pathogenesis of this syndrome.

Material And Methods: Thirty-three primary Sjögren's syndrome patients were included. Routine laboratory tests and immunological assessment (ANA, anti SS-A, anti SS-B antibodies, rheumatoid factor), ophthalmological assessment with ocular staining scoring, chest X-ray, and high-resolution computed tomography (if necessary) were performed. Serum concentrations of cytokines such as TGF-β, BAFF, APRIL, FLT-3L, LT-α, IL-21, and TNF-α were evaluated using standard ELISA assays. The histopathological evaluation (focus score) and the determination of CD3+, CD4+, CD19+, CD21+, CD35+ cells was performed.

Results: There was no significant correlation between TGF-β and other tested cytokines or autoantibodies, other than TNF-α. A negative correlation (ρ = -0.472) between TGF-β and TNF-α was found. There were no correlations between TGF-β and: results of ocular examinations, elements of histopathological variables, or lungs changes.

Conclusions: The authors state that: 1) the results may indicate that TGF-β influences the serum TNF-α activity in pSS patients, 2) our findings suggest that TGF-β may be the strongest inhibitor of TNF-α among cytokines involved in pSS pathogenesis, and 3) the results may explain the ineffectiveness of anti-TNF drugs in the treatment of pSS.

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