Main Article Content
Tumor necrosis factor -like weak inducer of apoptosis (TWEAK) triggers multiple cellular activities in a wide variety of cells, ranging from proliferation to cell death. It also causes upregulation of chemokine (C-X-C motif) receptor 5, and its ligand, chemokine (C-XC motif) ligand 13 (CXCL13). However, the precise roles of TWEAK and CXCL13 in the pathogenesis of SLE and their association with disease activity still obscure. The study included forty SLE patients and twenty control subjects. SLE disease activity was evaluated by Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) 2000 score. Anti-dsDNA antibodies, serum complement C3, highsensitivity CRP (hsCRP) concentrations, TWEAK and CXCL 13 serum concentrations were detected by ELISA. TWEAK mRNA expression in peripheral blood mononuclear cells was estimated by relative quantitative Real Time-PCR. Serum concentrations of TWEAK and CXCL13 were significantly elevated in SLE patients compared to controls (p < 0.05) with significant increase in patients with active SLE compared to those with inactive disease ( p< 0.05), they also significantly correlated with SLEDAI score and anti-dsDNA antibodies. TWEAK mRNA levels increased significantly in active lupus compared to inactive disease. It can be concluded that TWEAK serum and expression levels together with its inducible chemokine CXCL13 serum levels may benefit as biomarkers for prediction of SLE disease activity, as well as possible targets for personalized therapies due to their involvement in the pathogenesis of SLE.
Key words: Systemic lupus erythematosus (SLE); tumor necrosis factor-like weak inducer of apoptosis (TWEAK); (C-X-C motif) ligand 13 (CXCL13).