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- W4362508838 abstract "The receptor for advanced glycation end-products (RAGE) is a pattern recognition receptor that regulates inflammation, cell migration, and cell fate. Systemic lupus erythematosus (SLE) is a chronic multiorgan autoimmune disease. To understand the function of RAGE in SLE, we generated RAGE-deficient (Ager−/−) lupus-prone mice by backcrossing MRL/MpJ-Faslpr/J (MRL-lpr) mice with Ager−/− C57BL/6 mice. In 18-week-old Ager−/− MRL-lpr, the weights of the spleen and lymph nodes, as well as the frequency of CD3+CD4−CD8− cells, were significantly decreased. Ager−/− MRL-lpr mice had significantly reduced urine albumin/creatinine ratios and markedly improved renal pathological scores. Moreover, neutrophil infiltration and neutrophil extracellular trap formation in the glomerulus were significantly reduced in Ager−/− MRL-lpr. Our study is the first to reveal that RAGE can have a pathologic role in immune cells, particularly neutrophils and T cells, in inflammatory tissues and suggests that the inhibition of RAGE may be a potential therapeutic strategy for SLE." @default.
- W4362508838 created "2023-04-06" @default.
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- W4362508838 date "2023-05-01" @default.
- W4362508838 modified "2023-10-16" @default.
- W4362508838 title "Amelioration of nephritis in receptor for advanced glycation end-products (RAGE)-deficient lupus-prone mice through neutrophil extracellular traps" @default.
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