Decay accelerating factor regulates complement activation on glomerular epithelial cells

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

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55 Scopus citations

Abstract

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
Volume142
Issue number3
StatePublished - Jan 1 1989
Externally publishedYes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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    Quigg, R. J., Nicholson-Weller, A., Cybulsky, A. V., Badalamenti, J., & Salant, D. J. (1989). Decay accelerating factor regulates complement activation on glomerular epithelial cells. Journal of Immunology, 142(3), 877-882.