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

First Author  Lee J Year  2021
Journal  Sci Rep Volume  11
Issue  1 Pages  16348
PubMed ID  34381063 Mgi Jnum  J:359915
Mgi Id  MGI:6754970 Doi  10.1038/s41598-021-94855-5
Citation  Lee J, et al. (2021) Overexpression of cathepsin S exacerbates lupus pathogenesis through upregulation TLR7 and IFN-alpha in transgenic mice. Sci Rep 11(1):16348
abstractText  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-alpha, which leads to an autoimmune reaction and exacerbates lupus-like symptoms.
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