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Human macrophages kill human mesangial cells by Fas-L-induced apoptosis when triggered by antibody via CD16

J J Boyle1

  • 1Department of Histopathology, Faculty Of Medicine, Imperial College London, UK. joseph.boyle@imperial.ac.uk

Clinical and Experimental Immunology
|August 24, 2004
PubMed

Insights

Antibody-dependent cellular cytotoxicity (ADCC) involves macrophages inducing apoptosis in vascular smooth muscle cells and mesangial cells. This killing mechanism is mediated by Fas-L and CD16, crucial pathways in glomerulonephritis pathogenesis.

Area of Science:

  • Immunology
  • Cell Biology
  • Nephrology

Background:

  • Glomerulonephritis can result from antibody deposits activating macrophages, leading to tissue damage.
  • Macrophage-induced apoptosis of vascular smooth muscle cells (VSMCs) and mesangial cells (MCs) is implicated in glomerulonephritis.

Purpose of the Study:

  • To investigate antibody-dependent cellular cytotoxicity (ADCC) mediated by macrophages.
  • To elucidate the mechanisms of macrophage-induced apoptosis in VSMCs and MCs.

Main Methods:

  • Utilized U937 and primary human macrophages to study ADCC against human VSMCs and rodent MCs.
  • Employed biochemical assays (annexin-V, caspase-3, DNA content) and electron microscopy to confirm apoptosis.
  • Investigated the role of Fc-gamma receptors (CD16, CD64) and Fas-L in ADCC.

Main Results:

  • Antibody-activated macrophages induced apoptotic death in MCs and VSMCs.
  • Apoptosis was confirmed through multiple cellular and biochemical markers.
  • ADCC was significantly inhibited by blocking Fas-L and CD16 (Fc-gamma-RIII), but not CD64 (Fc-gamma-RI).

Conclusions:

  • Human macrophages induce apoptosis in human MCs via antibody-dependent cellular cytotoxicity (ADCC).
  • The Fas-L and CD16 (Fc-gamma-RIII) pathways are critical mediators of this macrophage-induced cell death.
  • These findings highlight potential therapeutic targets for antibody-mediated kidney diseases.

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