Treatment of lupus in NZB/W F1 mice with monoclonal antibody against Fas ligand

J Autoimmun. 2000 Mar;14(2):151-7. doi: 10.1006/jaut.1999.0356.


Since Fas ligand (FasL) can induce apoptosis of Fas-bearing cells, Fas/FasL interactions can play a critical role in maintaining self-tolerance. Fas/FasL interactions in lupus-like autoimmune disease have been well characterized in studies using either Fas or FasL mutant mice. However, the effect of the defective FasL-mediated signaling on the establishment of lupus in other mouse strains, such as NZB/W (B/W) F1, remains uncertain. In the present study, we examined the effect of anti-FasL monoclonal antibody (mAb) on the development of lupus. Treatment of B/W F1 mice with anti-FasL mAb augmented IgG1- and IgG2a-type anti-dsDNA Ab production. However, treatment of B/W F1 mice with anti-FasL mAb also significantly prevented the development of lupus nephritis. These results indicate that Fas/FasL interactions not only regulate IgG-type autoantibody production, but also influence the development of lupus nephritis in B/W F1 mice.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies, Antinuclear / blood
  • Antibodies, Monoclonal / therapeutic use*
  • Fas Ligand Protein
  • Female
  • Hybridization, Genetic
  • Immunoglobulin G / blood
  • Lupus Nephritis / blood
  • Lupus Nephritis / immunology*
  • Lupus Nephritis / prevention & control*
  • Lymphocyte Count
  • Membrane Glycoproteins / antagonists & inhibitors*
  • Membrane Glycoproteins / immunology
  • Mice
  • Mice, Inbred NZB


  • Antibodies, Antinuclear
  • Antibodies, Monoclonal
  • Fas Ligand Protein
  • Fasl protein, mouse
  • Immunoglobulin G
  • Membrane Glycoproteins