Abstract
Abstract Systemic lupus erythematosus (SLE) is autoimmune mediated chronic inflammatory diseases. Half of SLE patients suffer from lupus nephritis, and lupus nephritis is major cause of death in SLE. TWEAK/Fn14 interactions have been identified as pathologic factor in SLE pathogenesis. We conducted TWEAK/Fn14 pathway blocking by TWEAK receptor-Fc in SLE mice model and searched for the probable therapeutic mechanisms. CD19+ B cells were harvested from sanroque mice and TWEAK was administered. Sanroque mice were treated with TWEAK receptor-Fc or control-Fc for 3 weeks. Immunoglobulin (Ig) G, IgG1, IgG2a were measured in the sera of each group. Spleens from each group were stained with antibodies against CD4, B220, GL-7, CD138, and PD-1. Expression levels of mRNAs were determined by real-time PCR. Kidneys were stained with H&E and PAS. Administration of TWEAK promoted B cell differentiation. Treatment with TWEAK receptor-Fc suppressed the levels of IgG, IgG1, and IgG2a in sera and reduced B cell, plasma cell, follicular helper T cell (Tfh) in spleen of sanroque mice. Additionally, renal protective effects of TWEAK receptor-Fc were demonstrated. In conclusion, TWEAK receptor-Fc had beneficial effects on SLE mice model by repressing auto-reactive B cell, plasma cell, Tfh, and renal damage. In futher, TWEAK receptor-Fc would be a potential therapeutic agent in SLE patient.
Published Version
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