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Table 1 Summary of findings obtained using MPO-ANCA vasculitis animal models

From: In vivoapproaches to investigate ANCA-associated vasculitis: lessons and limitations

  Result Model Reference
Effector mechanisms    
   Neutrophil Neutrophil depletion abrogates crescentic glomerulonephritis. Mouse [24]
   T cells CD4+ effector T cells contribute to anti-MPO-mediated crescentic glomeruloneprhitis. Mouse (anti-GBM) [55]
  Th17 cells promote anti-MPO-mediated crescentic glomerulonephritis. Mouse (anti-GBM) [56]
   Proinflammatory stimuli Lipopolysaccharide aggravates crescentic glomerulonephritis in a TLR4-dependent manner. Mouse [25]
  Pertussis toxin/Mycobacterium tuberculosis aggravates crescentic glomerulonephritis. Rat [59]
   IgG glycosylation IgG glycan hydrolysis attenuates crescentic glomeruloneprhitis. Mouse [38]
   Leukocyte-endothelial interactions Anti-MPO IgG increases leukocyte adhesion and migration in cremasteric venules. Rat [20]
  Anti-MPO IgG increases leukocyte adhesion in glomerular capillaries. Mouse [27]
   Genetic susceptibility Rat and mouse strains differ in susceptibility to anti-MPO-mediated crescentic glomerulonephritis. Rat [59]
   Mouse [21]
Targets for treatment    
   Complement pathway Disruption of alternative complement pathway abrogates crescentic glomerulonephritis. Mouse [29]
  Genetic ablation of C5aR attenuates crescentic glomerulonephritis. Mouse (BM) [30]
   PI3Kγ signalling Genetic ablation of PI3Kγ attenuates crescentic glomerulonephritis. Mouse (BM) [33]
Experimental therapies    
   Anti-TNFα treatment Anti-TNFα pretreatment attenuates crescentic glomerulonephritis. Rat [32]
   Mouse [25]
   Anti-C5 treatment Anti-C5 pretreatment abrogates and treatment attenuates crescentic glomerulonephritis. Mouse [31]
   PI3Kγ inhibitor treatment Treatment with a PI3Kγ inhibitor attenuates crescentic glomerulonephritis. Mouse (BM) [33]
   P38 MAPK inhibitor treatment Treatment with a P38 MAPK inhibitor attenuates crescentic glomerulonephritis. Mouse [36]
  1. anti-GBM refers to the mouse model in which low-dose anti-glomerular basement membrane administration triggers disease in myeloperoxidase-immunized mice. BM refers to the bone marrow transplantation myeloperoxidase-anti-neutrophil cytoplasm autoantibody (MPO-ANCA) mouse model. C5aR, C5a receptor; MAPK, mitogen-activated protein kinase; PI3Kγ, phosphatidylinositol 3 kinase-gamma; Th17, T helper 17; TLR4, Toll-like receptor 4; TNFα, tumor necrosis factor-alpha. Adapted from [23].