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Published on: January 29, 2014
Complement-fixing activity of anticardiolipin antibodies in patients with and without thrombosis
M M Shinzato1, C Bueno, V S Trindade Viana
1Division of Rheumatology, University of São Paulo, Brazil. reumato@edu.usp.br
Insights
Complement-fixing anticardiolipin antibodies (C-fix aCL) are frequent in antiphospholipid syndrome (APS). While not distinguishing thrombotic risk, C-fix aCL may be more significant in venous events.
Area of Science:
- Immunology
- Rheumatology
- Vascular Medicine
Background:
- Anticardiolipin antibodies (aCL) are associated with antiphospholipid syndrome (APS).
- The complement-fixing activity of aCL (C-fix aCL) may play a role in thrombosis pathogenesis.
- Persistent moderate/high titres of IgG aCL antibodies are found in patients with and without thrombosis.
Purpose of the Study:
- To analyze the complement-fixing activity of anticardiolipin antibodies (C-fix aCL) in patients with antiphospholipid syndrome (APS) and persistent moderate/high IgG aCL titres.
- To compare C-fix aCL activity between patients with and without thrombotic events, and between arterial and venous events.
Main Methods:
- In vitro analysis of complement-fixing activity of anticardiolipin antibodies (C-fix aCL).
- Measurement of aCL titre and C-fix ability using ELISA.
- Comparison of IgG aCL levels, IgM aCL frequency, and C-fix aCL frequency and titre between patient groups.
Main Results:
- High frequency of C-fix aCL observed in both APS and non-APS patients with moderate/high IgG aCL titres (71% vs. 92%).
- No significant difference in mean IgG aCL titre, IgM aCL frequency, or mean C-fix aCL level between APS and non-APS patients.
- A trend towards higher frequency and significantly higher titre of C-fix aCL was observed in patients with exclusive venous events compared to those with exclusive arterial events (p=0.07 and p=0.016, respectively).
Conclusions:
- Complement-fixing anticardiolipin antibodies (C-fix aCL) are highly prevalent in patients with antiphospholipid syndrome (APS).
- C-fix aCL does not discriminate patients with persistent moderate/high aCL levels but without thrombotic events.
- The complement-fixing property of aCL appears more relevant in venous events, suggesting distinct pathogenic mechanisms in arterial versus venous occlusive disorders of APS.
Abstract:
We have analysed in vitro the complement-fixing activity of anticardiolipin antibodies (C-fix aCL) from patients with persistent and moderate/high titres IgG aCL antibodies: 21 with thrombosis and 11 without thrombosis. Titre and C-fix ability of aCL were measured by ELISA. APS and non-APS patients were similar with regard to mean levels of IgG aCL (46 +/- 24 versus 51 +/- 30 GPL, P = 0.7), frequency of IgM aCL (P = 0.7) and a comparable predominance of IgG2 aCL reactivity on ELISA (95% versus 100%, respectively, P = 1.0). Remarkably, a high frequency of C-fix aCL (71% versus 92%, P = 0.35) was observed in both groups. Similarly, no difference was observed in the mean level of C-fix aCL in APS and non-APS patients (7 +/- 6 versus 9 +/- 8 SDunits, P = 0.3). Analysis of 10 primary and 11 secondary APS also revealed a comparable IgG aCL mean titre (57 +/- 29 versus 37 +/- 11, P = 0.06), frequency of IgM aCL (P = 0.6) and of C-fix aCL (70% versus 73%, P = 0.99). Among APS patients six had exclusive arterial events and seven exclusive venous events. The IgG aCL mean titre (36 +/- 10 versus 36 +/- 11 GPL, P = 0.9) and the frequency of IgM aCL antibodies (P = 0.56) in these subgroups of patients were comparable. There was a trend of higher frequency of C-fix aCL in patients with exclusive venous events (100%) compared to 50% of those with exclusive arterial events (p = 0.07). Importantly, C-fix aCL titre was higher in the former group compared to the later one (8 +/- 5 SDunits versus 2 +/- 2 SDunits, P = 0.016). Our data support the notion of a high frequency of C-fix aCL in APS. Although it does not discriminate those patients without thrombotic events with persistent moderate/high levels of aCL, this property seems to be more relevant in venous events and may provide the basis for further understanding the distinct pathogenic mechanisms underlying arterial and venous occlusive disorders of APS.
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