Soluble Receptor Level of Advanced Glycation (sRAGE) Products in Serum in Patients with Systemic Lupus Erythematosus:

Abstract

Introduction: Systemic Lupus Erythematosus (SLE) is an autoimmune disease characterized by antibody formation against nuclear autoantigens. Many molecules play a role in etiopathogenesis. A receptor for Advanced Glycation (RAGE) is produced by many immune system cells, such as neutrophils, macrophages, and T cells, and interacts with many classes of ligands. For example, studies have shown that the interaction of the receptor with the HMG1 (High mobility group box-1) ligand induces the production of type 1 interferon (IFN), which plays a crucial role in the pathogenesis of SLE. In light of these results, the level of sRAGE, the soluble form of RAGE, may be associated with disease activity. In light of this information, we aimed to evaluate whether there is a relationship between plasma sRAGE levels and SLE. Methods: Eighteen patients diagnosed with SLE (M/F: 1/17) and twenty-one patients without any disease diagnosis (M/F: 2/19) were included as the control group. Four patients were classified as inactive SLE and fourteen as active SLE according to the SLE Disease Activity Index (SLEDAI) classification criteria. In these patients, plasma sRAGE level was measured by ELIZA method using ELIZA (enzyme-linked immunosorbent assay) kit (BioVendor Research and Diagnostic Products). The data obtained were compared between the groups. Conclusion: The mean plasma sRAGE level was lower in patients with SLE than in healthy control patients but not statistically significant (p=0.966). Our study found a positive correlation between SLEDAI and sRAGE levels in patients with SLE (r=0.628, p=0.005). Although no significant correlation was found between patients with SLE, sRAGE levels were positively correlated between fourteen patients classified as active SLE and the control group. sRAGE levels were statistically significantly higher in patients with active SLE (r=0.695, p=0.001). Discussion: In our study, we found that plasma sRAGE levels in patients with SLE were lower than in healthy controls, but plasma sRAGE levels in patients with active SLE were higher than plasma sRAGE levels in patients with inactive SLE. We hypothesized that reduced sRAGE levels in patients with SLE could be explained by the depletion of this soluble receptor. sRAGE-ligand complexes have been suggested to be eliminated from the blood via the spleen and liver. It is also possible that sRAGE levels in SLE patients are adjusted by alternative splicing and proteinases, and this possibility needs to be clarified in future investigations. Our study differed from another similar study showing that blood sRAGE levels were higher in patients with SLE than in healthy controls. Blood sRAGE levels were significantly increased during active disease compared with patients with quiescent SLE. The medication use of the patients and the small number of patients may explain this discrepancy.