Circulating sTWEAK and its scavenger receptor sCD163 concentrations in patients with Behçet’s Disease

Abstract

Circulating sTWEAK and its scavenger receptor sCD163 concentrations in patients with Behçet's disease B ehçet's disease (BD) is a chronic multisystemic inflammatory disorder with major clinical manifestations including recurrent oral and genital aphthous ulcerations and eye and skin lesions [1]. BD shares some common features with autoinflammatory and autoimmune diseases and MHC-Iopathy [2]. Although its etiology and pathogenesis are not known precisely, several triggering factors such as infectious agents and/or immunological insults may induce inflammatory attacks in genetically predisposed individuals [2,3]. It has been thought that inflammation, which is a hallmark of BD manifestations, involves the activation of several cell types like neutrophils, B cells, a variety of T cells, and production of cytokines, chemokines, and adhesion molecules, tissue factor expression, and microparticles [4][5][6]. Tumor necrosis factor (TNF)-alpha, interferon-gamma, and members of the interleukin family are among the major inflammatory cytokines investigated in this context [7][8][9][10]. Proinflammatory cytokine soluble TNF-like weak inducer of apoptosis (TWEAK), which belongs to the TNF superfamily, is associated with many different inflammatory disorders [11][12][13][14][15]. TWEAK (30 kD, 249 aa), which is synthesized as a membranebound protein in the endoplasmic reticulum, is processed Objectives: Behçet's disease (BD) is a chronic multisystemic inflammatory disorder and is associated with many inflammatory processes. The present study aimed to examine the serum levels of proinflammatory cytokine soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) and its scavenger receptor soluble cluster of differentiation 163 (sCD163) simultaneously in patients with BD by considering their relationships with disease activity. Methods: The study group included 53 patients with BD (29 females and 24 males) and 30 healthy individuals. Patients with a lesion or active organ involvement were defined as active (n=39) and those without were identified as inactive (n=14). Serum sTWEAK and sCD163 concentrations were determined by enzyme-linked immunosorbent assay. Results: Serum sTWEAK and sCD163 levels were significantly increased in patients with BD compared with the healthy group (p=0.016 and p=0.003, respectively). Concentrations of these two molecules were also higher in active and inactive BD than the healthy individuals (p=0.043 for sTWEAK and p=0.010 for sCD163). Receiver operating characteristic curve analysis revealed that serum sCD163 and sTWEAK levels had a discriminating ability between patients with BD and healthy controls with area under the curve values of 0.706 and 0.661, respectively. Conclusion: It was concluded that circulating sTWEAK and its scavenger receptor sCD163 levels were increased in BD, significantly predicted the disease, and might be significant molecules to assess inflammation.