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, and induced lupus-like symptoms. Eight months later, the TG mice spontaneously developed typical SLE symptoms regardless of the inducement. Furthermore, we observed increased toll-like receptor 7 (TLR7) expression with increased monocyte and neutrophil populations in the TG mice. In conclusion, overexpression of CTSS in mice influences TLR7 expression, autoantibodies and IFN-α, which leads to an autoimmune reaction and exacerbates lupus-like symptoms.
Highlights
Systemic lupus erythematosus (SLE) is a chronic inflammatory disease commonly observed in w omen[1,2]
The expression of human Cathepsin S (CTSS) is exceptionally high in all organs of TG female mice in comparison with wild type (WT) female mice
The mRNA level of CTSS was significantly high in the kidneys, lymph nodes, spleen and skin, a condition known as organ-affected SLE (Fig. 1b)
Summary
Systemic lupus erythematosus (SLE) is a chronic inflammatory disease commonly observed in w omen[1,2]. To investigate the SLE in the murine model, the natural hydrocarbon oil obtained from shark liver named 2,6,10,14-tetramethylpentadecane (TMPD, commonly known as pristane) is used[11,12]. It stimulates the secretion of IFN-α through monocytes and leads to indirect activation of T LR713. CTSS cleaves various proteins and components of the basal membrane[17,18] Due to these activities, CTSS production can lead to immune cell infiltration into peripheral vascular regions, triggering a vigorous immune response[19,20,21,22,23]
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