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Related Experiment Videos

Decay-accelerating factor but not CD59 limits experimental immune-complex glomerulonephritis.

Lihua Bao1, Mark Haas, Andrew W Minto

  • 1Section of Nephrology, The University of Chicago, Chicago, IL 60637, USA. lbao@medicine.bsd.uchicago.edu

Laboratory Investigation; a Journal of Technical Methods and Pathology
|January 30, 2007
PubMed
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Deficiency in decay accelerating factor (DAF) exacerbates immune complex-mediated glomerulonephritis (ICGN) by increasing C3 deposition. CD59 deficiency did not impact disease, suggesting C3 activation is key in this ICGN model.

Area of Science:

  • Immunology
  • Nephrology
  • Complement System Biology

Background:

  • The complement system plays a dual role in immune complex-mediated glomerulonephritis (ICGN), with both activating and regulatory proteins influencing disease pathogenesis.
  • Decay accelerating factor (DAF) and CD59 are key regulators, inhibiting C3 activation and C5b-9 generation, respectively.
  • These proteins are widely distributed cell membrane proteins crucial for immune regulation.

Purpose of the Study:

  • To investigate the role of DAF and CD59 in the development of experimental ICGN.
  • To determine the relative importance of C3 activation versus C5b-9 generation in ICGN pathogenesis.
  • To assess the impact of DAF and CD59 deficiency on glomerular inflammation and injury.

Main Methods:

  • Induction of chronic serum sickness and ICGN in DAF-deficient, CD59-deficient, and DAF/CD59-deficient mice.

Related Experiment Videos

  • Comparison of disease incidence and severity with wild-type littermate controls.
  • Analysis of glomerular C3 deposition, monocyte chemoattractant protein-1 mRNA expression, and leukocyte infiltration.

    • Main Results:

    • DAF-deficient and DAF/CD59-deficient mice exhibited a higher incidence of glomerulonephritis (GN) with increased glomerular C3 deposition compared to controls.
    • CD59-deficient mice showed no significant difference in disease expression compared to wild-type mice.
    • DAF-deficient mice displayed elevated monocyte chemoattractant protein-1 mRNA and increased glomerular leukocyte infiltration.

    Conclusions:

    • C3 activation is strongly implicated in the pathogenesis of experimental ICGN.
    • The terminal complement pathway component C5b-9 appears to have a lesser pathogenic role in this specific ICGN model.
    • DAF deficiency significantly contributes to the development of ICGN, highlighting its regulatory importance.