Decay accelerating factor regulates complement activation on glomerular epithelial cells

R. J. Quigg, A. Nicholson-Weller, A. V. Cybulsky, J. Badalamenti, D. J. Salant

Research output: Contribution to journalArticlepeer-review

68 Scopus citations


Epithelial cells of the glomerular capillary are the site of C5b-9 mediated injury in rat membranous nephropathy. We investigated the regulation of C activation by cultured glomerular epithelial cells (GEC). Rat and human GEC were more resistant to C injury by homologous C than heterologous C. In human GEC homologous C cytotoxicity was enhanced by antiserum to decay accelerating factor (DAF) indicating that homologous C activation was, at least in part, restricted by membrane DAF. Anti-DAF immunoprecipitated a 67-kDa protein from human glomeruli. In rat GEC, pronase and phosphatidylinositol-specific phospholipase C (which are known to inactivate human DAF) enhanced cytotoxicity by homologous C. Thus, DAF is present on human GEC in culture and in human kidney glomeruli, and a DAF-like protein is present on cultured rat GEC. These proteins regulate C activation in vitro and may play a role in controlling C activation on GEC in vivo.

Original languageEnglish (US)
Pages (from-to)877-882
Number of pages6
JournalJournal of Immunology
Issue number3
StatePublished - 1989
Externally publishedYes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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