MedicineImmunologyNephrologyImmunopathologyInflammationRenal PathophysiologyComplement RegulationComplement SystemImmune-mediated Renal DiseaseNephritic SyndromeRenal ImmunopathologyRenal InflammationActivationC3 Complement LevelsC3 ConvertaseComplement In Renal DiseaseRenal Complement InjuryTerminal Complement Complex
Plasma samples from patients with nephritic factor (NeF) were examined for their C3 converting activity. C3, C3dg, C5 and the fluid phase terminal complement complex (TCC) were quantified. All patients had evidence of C3 activation with low plasma C3 and high C3dg. Some patients had normal C5 and normal TCC levels, and thus no evidence of terminal pathway activation in vivo; others, with slower C3 conversion in vitro, had low C5 levels with TCC either elevated or in the upper normal range, suggesting in vivo activation of the terminal pathway. These observations were confirmed by in vitro experiments using purified NeFs. It is concluded that considerable activation of C3 may occur in vivo without a simultaneous activation of the terminal pathway, and that NeF is heterogeneous with regard to its ability to activate complement.
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Tom Eirik Mollnes, Tor Lea, Stig S. Frøland et al. · Scandinavian Journal of Immunology · 1985 · 349 citations
Life Sciences, Immunology, Pathology +11