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Category:Computer-aided design software Category:1993 software Category:Graphical user interfaces Category:3D graphics software Category:Technical communication tools Category:Windows multimedia software Category:UNICOS software Category:Technical communication tools Category:MIDlets Category:Technical communication toolsRelevance of CXCL16/DC-CXCR6 axis in pathogenesis of systemic lupus erythematosus (SLE): a significant effect of CXCL16 knockdown on SLE. Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with a complex pathogenesis. The expression of chemokine (C-X-C motif) ligand 16 (CXCL16) is known to be involved in the pathogenesis of SLE. The main receptor of CXCL16 is chemokine (C-X-C motif) receptor 6 (CXCR6). The aim of this study was to evaluate the potential effect of CXCL16 on SLE via its receptor. SLE is characterized by the production of autoantibodies. In order to investigate whether CXCL16 is involved in the pathogenesis of SLE, the expression of CXCL16 and CXCR6 was evaluated in the serum of patients with SLE and healthy subjects (HS). The effects of CXCL16 on the proliferation, apoptosis and differentiation of PBMCs in SLE were also determined. The expression of CXCL16 and CXCR6 was significantly higher in the serum of SLE patients than in HS. The expression of CXCL16 and CXCR6 was positively correlated with the SLE disease activity index (SLEDAI) and negatively correlated with disease activity. Knockdown of CXCL16 by short-interfering RNA (siRNA) decreased the proliferation of SLE PBMCs in vitro. CXCL16 knockdown also increased the apoptosis of SLE PBMCs. After knockdown of CXCL16, the expression of interferon (IFN)-α and IFN-β was decreased. Knockdown of CXCL16 suppressed the differentiation of CD4+ T cells into Th1 and Th17 cells. CXCL16 knockdown significantly ameliorated lupus nephritis in the MRL/lpr/lpr mouse model. CXCL16 knockdown supp e315de8065
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