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Updated: Sep 25, 2026

Ferric Chloride-induced Murine Thrombosis Models
Published on: September 5, 2016
A thrombin-cross-reactive anticardiolipin antibody binds to and inhibits the anticoagulant function of activated
Kwan-Ki Hwang1, Cheng-De Yang, Weihong Yan
1Medicine/Rheumatology, University of California, Los Angeles, CA 90095-1670, USA. hwangkk@ucla.edu
Insights
Some anticardiolipin antibodies (aCL) bind to protein C (PC) and activated PC (APC). One specific aCL inhibited APC
Area of Science:
- Immunology
- Hematology
- Thrombosis Research
Background:
- Anticardiolipin antibodies (aCL) are associated with thrombosis.
- The interaction of aCL with protein C (PC) and activated PC (APC) is not fully understood.
Purpose of the Study:
- To investigate if thrombin-reactive aCL bind to PC and/or APC.
- To determine if these binding aCL affect PC activation or APC function.
Main Methods:
- Studied patient-derived monoclonal aCL reactivity with PC and APC.
- Assessed the impact of reactive antibodies on PC activation and APC activity in plasma.
Main Results:
- Five of five thrombin-reactive monoclonal aCL bound to PC and APC.
- One antiprothrombin antibody with aCL activity also bound to PC and APC.
- One antibody (CL15) inhibited the anticoagulant function of APC.
Conclusions:
- Thrombin-reactive aCL frequently bind to PC and APC in antiphospholipid syndrome.
- Some APC-reactive aCL may inhibit APC's anticoagulant function, potentially promoting thrombosis.
Objective:
To test the hypotheses that some thrombin-reactive anticardiolipin antibodies (aCL) may bind to protein C (PC) and/or activated PC (APC), and that some of the PC- and APC-reactive aCL may inhibit PC activation and/or the function of APC.
Methods:
We studied the reactivity of patient-derived monoclonal aCL with PC and APC. We examined the effects of the reactive antibodies on PC activation and on the activity of APC in plasma coagulation.
Results:
Five of 5 patient-derived, thrombin-reactive monoclonal aCL bound to PC and APC. In addition, 1 patient-derived monoclonal antiprothrombin antibody (APT) that displayed aCL activity and reacted with thrombin also bound to PC and APC. Of these 6 PC- and APC-reactive aCL/APT, all failed to inhibit PC activation, but 1 (CL15) shortened the plasma coagulation time in the presence of exogenous APC and thus inhibited the anticoagulant function of APC.
Conclusion:
Most of the thrombin-reactive aCL in patients with antiphospholipid syndrome may bind to PC and APC. Of the APC-reactive aCL, some (like CL15) may inhibit the anticoagulant function of APC and are thus likely to be prothrombotic in the host.
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