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Interleukin-37 (IL-37) exerts broad inhibitory properties on the innate inflammatory and acquired immune responses. This study was set up to investigate the expression of IL-37 in Behçet disease (BD) and to explore its possible regulatory role during inflammation. IL-37 protein levels and mRNA expression in lipopolysaccharides (LPS)-stimulated peripheral blood mononuclear cells (PBMCs) from 50 BD (30 patients in active stage) patients and 20 healthy controls were assayed by real-time polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). Cytokines in the serum and the supernatants of stimulated PBMCs and CD4(+) T cells were assayed by ELISA. Active BD patients showed a decreased IL-37 expression and increased IL-1β, IL-6, and tumor necrosis factor-alpha (TNF-α) levels in serum and in PBMC culture supernatants. Active BD patients treated with corticosteroids showed an enhanced IL-37 production. Recombinant IL-37 (rIL-37) induced a significant decrease of inflammatory cytokines (IL-1β, IL-6, and TNF-α). It also markedly decreased IL-17 expression in PBMCs and CD4(+) T cells from active BD patients. The present study suggests that a decreased IL-37 expression in BD patients is associated with an increased inflammatory response. Corticosteroid treatment of active BD patients is associated with an increased expression of IL-37 mRNA, which suggests that treatment may partly exert its immunosuppressive effect by regulating IL-37 production and reducing inflammatory cytokines.

Behcet's disease (BD) is a multi-systemic inflammatory disorder characterized by the "triple symptom complex". Several pro-inflammatory cytokines, mainly derived from the immune Th17 axis, seem to be involved in different pathogenic pathways leading to development of the clinical manifestations. Here, we have analyzed the expression and role of IL-26 in active BD patients, an inflammatory disorder characterized by bronchoalveolar lavage fluid (BAL) and cerebrospinal fluid (CSF) inflammation. On this basis, the primary aim of our work was to study IL-26 levels in serum, BAL CSF) from active BD patients. Samples were collected from 95 BD patients (55 patients were in active stage) and 50 healthy controls (HC). They were investigated with ELISA for estimation of cytokines levels. Serum concentration of IL-26 resulted higher in both active [4.80±1.32] and inactive [2.77±1.026] BD than HC [0.31±0.14ng/ml; p

Since the discovery of interleukin-33 (IL-33) ligand for the ST2 receptor, scarce studies have implicated this cytokine in the pathogenesis of Behcet's disease (BD). IL-33 is member of the IL-1 superfamily of cytokines that is expressed by epithelial cells, endothelial cells, inflammatory cells and central nervous tissue. Its expression is upregulated following pro-inflammatory situations making IL-33 essential to innate immunity. IL-33 can function both as a traditional cytokine and as a nuclear factor regulating gene transcription. It is thought to function as an "alarmin" which is released following cell necrosis to alert the immune system of tissue damage or stress. This short review highlights the emerging roles of IL-33 protein and raises many interrogations about its involvement in BD.