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.
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.
Authors: M Galli; P Comfurius; C Maassen; H C Hemker; M H de Baets; P J van Breda-Vriesman; T Barbui; R F Zwaal; E M Bevers Journal: Lancet Date: 1990-06-30 Impact factor: 79.321
Authors: R M Bertina; B P Koeleman; T Koster; F R Rosendaal; R J Dirven; H de Ronde; P A van der Velden; P H Reitsma Journal: Nature Date: 1994-05-05 Impact factor: 49.962
Authors: Cai-Sheng Lu; Arash A Horizon; Kwan-Ki Hwang; John FitzGerald; Wei-Shiang Lin; Bevra H Hahn; Daniel J Wallace; Allan L Metzger; Michael H Weisman; Pojen P Chen Journal: Arthritis Rheum Date: 2005-12
Authors: Bahar Artim-Esen; Charis Pericleous; Ian Mackie; Vera M Ripoll; David Latchman; David Isenberg; Anisur Rahman; Yiannis Ioannou; Ian Giles Journal: Arthritis Res Ther Date: 2015-03-07 Impact factor: 5.156