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Decay accelerating factor regulates complement activation on glomerular epithelial cells.

R J Quigg1, A Nicholson-Weller, A V Cybulsky

  • 1Evans Memorial Department of Clinical Research, University Hospital, Boston, MA 02118.

Journal of Immunology (Baltimore, Md. : 1950)
|February 1, 1989
PubMed
Summary
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Glomerular epithelial cells (GEC) protect themselves from complement-mediated injury. Decay accelerating factor (DAF) on GEC regulates complement activation, preventing damage to these kidney cells.

Area of Science:

  • Nephrology
  • Immunology
  • Cell Biology

Background:

  • Glomerular epithelial cells (GEC) are implicated in complement-mediated injury during membranous nephropathy.
  • Understanding the regulation of complement (C) activation on GEC is crucial for understanding kidney disease pathogenesis.

Purpose of the Study:

  • To investigate the regulation of complement activation by cultured glomerular epithelial cells (GEC).
  • To determine the role of decay accelerating factor (DAF) in protecting GEC from complement-mediated injury.

Main Methods:

  • Cultured rat and human GEC were exposed to homologous and heterologous complement.
  • Cytotoxicity assays were performed with and without antiserum to decay accelerating factor (DAF).
  • Biochemical analysis, including anti-DAF immunoprecipitation and treatment with pronase and phosphatidylinositol-specific phospholipase C, was used.

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Main Results:

  • Both rat and human GEC exhibited resistance to homologous complement injury compared to heterologous complement.
  • In human GEC, antiserum to DAF enhanced homologous complement cytotoxicity, indicating DAF's inhibitory role.
  • DAF-like proteins were identified on both human and rat GEC, regulating complement activation in vitro.

Conclusions:

  • Decay accelerating factor (DAF) is present on human GEC and glomeruli, and a DAF-like protein exists on rat GEC.
  • These membrane-bound proteins play a significant role in regulating complement activation on GEC.
  • DAF likely contributes to protecting GEC from complement-mediated injury in vivo.