Ontology highlight
ABSTRACT:
SUBMITTER: Barbour TD
PROVIDER: S-EPMC4869622 | biostudies-literature | 2016 Apr
REPOSITORIES: biostudies-literature
Barbour Thomas D TD Ling Guang Sheng GS Ruseva Marieta M MM Fossati-Jimack Liliane L Cook H Terence HT Botto Marina M Pickering Matthew C MC
Kidney international 20160203 4
C3 glomerulopathy is a complement-mediated renal disease that is frequently associated with abnormalities in regulation of the complement alternative pathway. Mice with deficiency of factor H (Cfh(-/-)), a negative alternative pathway regulator, are an established experimental model of C3 glomerulopathy in which complement C3 fragments including iC3b accumulate along the glomerular basement membrane. Here we show that deficiency of complement receptor 3 (CR3), the main receptor for iC3b, enhance ...[more]