Differential Expression of Suppressor of Cytokine Signalling Proteins in Behçet's Disease. (November 2014)

• Record Type: Journal Article
• Authors: Hamedi, M.; Bergmeier, L. A.; Hagi‐Pavli, E.; Vartoukian, S. R.; Fortune, F.
• Is Part Of: Scandinavian journal of immunology. Volume 80:Number 5(2014:Nov.)
• Page Start: 369
• Page End: 376
• Publication Date: 2014-11
• Subjects: Immunology -- Periodicals; 571.96
• DOI: 10.1111/sji.12211
• Languages: English
• ISSNs: 0300-9475

Abstract

<abstract abstract-type="main" id="sji12211-abs-0001"> <title>Abstract</title> <p>Behçet's disease (BD) is a chronic, multisystemic, recurrent vasculitis disease of unknown aetiology. Proinflammatory cytokines are a key feature of the disease, but the triggers for their induction are not well understood and/or controversial. Suppressor of cytokine signalling (SOCS) proteins which negatively regulate the JAK–STAT signalling pathway of cytokine induction may be dysregulated in BD. The expression of SOCS1 and 3 mRNA and protein was studied in peripheral blood mononuclear cells (PBMCs) and neutrophils of patients with BD and compared with healthy controls (HCs) and patients with recurrent aphthous stomatitis (RAS) using RT‐PCR, Western blot and immunohistochemistry. SOCS1 and 3 mRNA was also measured in buccal mucosal cells (BMC) of patients with BD and HCs. SOCS1 and 3 mRNA was significantly upregulated in PBMCs of patients with BD compared with HCs (<italic>P</italic> = 0.0149; <italic>P</italic> = 0.0007). In addition, there were subtle differences between expression in active and symptom‐free BD (quiescent BD). SOCS1 and SOCS 3 were also significantly upregulated in BMC from oral ulcers of BD compared with HCs (both at <italic>P</italic> = 0.0001). A differential expression of both SOCS1 and 3 was observed between PBMCs and neutrophils in patients with BD. Immunohistochemical analysis revealed differential expression of SOCS proteins in the buccal mucosa with an increased expression at the ulcer surface of ulcers than in the non‐ulcerated tissue. These observations suggest a dysregulation of the expression of these important regulators not only between patients with BD and healthy controls but also between mucosal and systemic tissues, which may reflect the nature of the aetiopathology of the disease.</p> </abstract>