Glomerular deposition of galactose-deficient IgA1-containing immune complexes via glomerular endothelial cell injuries.
Yuko MakitaHitoshi SuzukiDaisuke NakanoHiroyuki YanagawaToshiki KanoJan NovakAkira NishiyamaYusuke SuzukiPublished in: Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association (2022)
Gd-IgA1-IgG ICs had a high affinity for glomerular endothelial cells, which resulted in glomerular filtration barrier dysfunction mediated by glycocalyx loss. Furthermore, Gd-IgA1-IgG ICs accelerated the production of adhesion factors and proinflammatory cytokines in glomerular endothelial cells. The glomerular endothelial cell injury induced by Gd-IgA1-containing ICs may enhance the permeability of Igs in the mesangial region and subsequent inflammatory responses in the pathogenesis of IgAN.