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Respective roles of decay-accelerating factor and CD59 in circumventing glomerular injury in acute nephrotoxic serum

Feng Lin1, David J Salant, Howard Meyerson

  • 1Institute of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|February 7, 2004
PubMed

Insights

Decay-accelerating factor (DAF) is crucial for protecting kidneys from immune-mediated injury. Loss of DAF, but not CD59, significantly worsens nephritis by increasing complement deposition and podocyte damage.

Area of Science:

  • Nephrology
  • Immunology
  • Complement System

Background:

  • Decay-accelerating factor (DAF) and CD59 regulate complement activation.
  • Their specific roles in protecting glomeruli during immune-mediated nephritis are not well understood.

Purpose of the Study:

  • To investigate the in vivo roles of DAF and CD59 in protecting glomeruli during nephrotoxic serum (NTS) nephritis.

Main Methods:

  • Induction of NTS nephritis in wild-type, Daf1(-/-), CD59a(-/-), and Daf1(-/-)CD59a(-/-) mice.
  • Assessment of proteinuria, histology, immunohistochemistry, and electron microscopy of kidneys.

Main Results:

  • Daf1(-/-) mice exhibited severe albuminuria and podocyte foot process effacement post-NTS induction.
  • Albuminuria and glomerular damage were significantly exacerbated in Daf1(-/-)CD59a(-/-) mice.
  • C3 and C9 deposition were markedly increased in Daf1(-/-) and double knockout mice.

Conclusions:

  • DAF is the primary regulator protecting glomeruli from classical pathway-mediated injury in autoantibody-induced nephritis.
  • CD59 plays a secondary role in limiting C5b-9-mediated cell damage.

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