Acute serum sickness in normal and C6 deficient rabbits: Role of membrane attack complex

G. Parra, Y. Takekoshi, J. Striegel, R. L. Vernier, A. F. Michael

Research output: Articles / NotesScientific Articlepeer-review

5 Scopus citations


Acute serum sickness was induced in New Zealand White (NZW) and in C6 deficient (C6D) rabbits, to compare the histology, immunofluorescence, especially distribution of poly C9 (MAC), and electron microscopic characteristics of the disease in each strain. Glomerulonephritis and albuminuria of comparable extent occurred in 13/17 NZW and 4/8 C6D rabbits. In NZW rabbits with albuminuria an early intense glomerular infiltration by mononuclear cells was associated with focal small fine granular glomerular basement membrane (GBM) deposits of IgG and BSA and more diffuse and larger deposits of C3 and MAC. After the disappearance of monocytes and decrease in mesangial cell proliferation, development of large subepithelial GBM deposits rich in all immune reactants was observed in NZB rabbits. In C6D rabbits with albuminuria a similar monocytic infiltrate occurred, but no association with IgG and C3 GBM immune deposits was noted. No deposits of MAC and no large subepithelial GBM 'humps' were observed in C6D rabbits. We conclude that the exudative (monocytic) phase of glomerular injury and albuminuria in acute serum sickness nephritis are not dependent upon terminal complement components, but the subsequent formation of large subepithelial GBM deposits does not occur in this model in the absence of MAC.

Original languageEnglish
Pages (from-to)299-312
Number of pages14
JournalInternational Journal of Experimental Pathology
Issue number3
StatePublished - 1992
Externally publishedYes


  • C-6 deficiency
  • Glomerulonephritis
  • Membrane attack complex
  • Rabbits


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