In addition, complement activation on platelets may be caused by Ruxolitinib phosphate platelet activation and subsequent exposure of C1q binding epitopes on the activated platelet cell surface. Currently, it is unclear which of these mechanisms, autoantibody-mediated complement activation or direct binding of C1q due to platelet activation, is operating in SLE to increase platelet complement deposition. Complement Penicillin G Sodium deposition on platelets has been seen in cases of individuals with stroke, but is otherwise thought to be specific for SLE, although studies have not been extensive in other chronic inflammatory diseases. In SLE, increased C4d deposition on platelets is associated with vascular events. However, there are discrepancies in the literature as to whether it is venous or arterial vascular events which are associated with complement deposition on platelets. In addition it is also important to note that none of the previous investigations adjusted data for traditional cardiovascular risk factors. The aim of this study was to investigate if aPL antibodies could support classical pathway activation on platelets in vitro as well as in SLE patients. Furthermore, in data which had been adjusted to account for traditional cardiovascular risk factors and aPL antibodies, we investigated with which kind of vascular events, arterial or venous, complement deposition on platelets was associated. Finally, we analyzed if deposition of complement factors C1q and C4d on platelets was specific for SLE or also found in disease controls and healthy individuals. In brief we found that aPL antibodies supported activation of the classical pathway of the complement system on platelets by two separate mechanisms; amplification of platelet activation, and by providing complement-fixing antibodies on the platelet surface. Platelet activation was analyzed by flow cytometry measuring platelet Pselectin and CD69 expression. CD69 is constitutively expressed on platelets, but is increased upon activation and is important for platelet aggregation. In SLE patients, deposition on platelets of both complement factor C1q and C4d, was associated with venous, but not arterial, thrombosis when the data was adjusted to account for traditional cardiovascular risk factors and aPL antibodies. These results suggest a possible link between aPL antibodies and development of venous thrombosis through mechanisms involving complement activation on platelets.