Overexpression of cathepsin S exacerbates lupus pathogenesis through upregulation TLR7 and IFN-α in transgenic mice

Abstract Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that affects multiple organs. Recent studies suggest relevance between cysteine protease cathepsin S (CTSS) expression and SLE. To investigate the mechanism of CTSS in SLE, CTSS-overexpressing transgenic (TG) mice were generated, induced lupus-like symptoms. Eight months later, TG spontaneously developed typical SLE symptoms regardless inducement. Furthermore, we observed increased toll-like receptor 7 (TLR7) with monocyte neutrophil populations mice. In conclusion, overexpression influences TLR7 expression, autoantibodies IFN-α, which leads to an reaction exacerbates