The role of LIGHT in the pathogenesis of glomerulonephritis

点击翻译按钮获取中文摘要

LIGHT, a member of TNF superfamily, has been reported to play a important role for costimulatory molecules in T cell activation and expansion. Previous studies have shown that treatment of rodents with a lymphotoxin (LT) beta receptor-Ig fusion protein (LTbetaR-Ig), which binds to both LT and LIGHT, prevents the development of Tcell-mediated autoimmune diseases. In addition, dysregulated T cell-derived LIGHT lead to pathological features similar to those of human IgA nephropathy (IgAN). These data raise the possibility that LIGHT is involved in the pathogenesis of glomerulonephritis, e.g, IgAN or crescentic glomerulonephritis. The aim of this study is to explore the involvement of LIGHT in the pathogenisis of glomerulonephritis by using experimental autoimmune anti-glomerular basement membranenephritis (EAG) or murin IgA nephropathy model. For this purpose, we generated LTbetaR-Ig and verified whether LTbetaR-Ig treatment prevents EAG induced in WKY rats by immunization with an nephritogenic peptide, recombinant alpha 3(IV)NC1 of type IV collagen. Rats injected with nephritogenic antigen showed heavy proteinuria and crescent formation in 80 to 100% of the glomeruli as shown previously, but there was no significant difference between LTbetaR-Ig-treament and non-treatment groups in our study.