Inhibitory and activating human antiplatelet antibodies

Platelets are essential for the maintenance of haemostasis and, on the other hand, play a pivotal role in the formation of a thrombus. It is clear that reduced platelet activity will result in a bleeding tendency, whereas stimulation of platelets can lead to thrombosis. Human antiplatelet antibodies may not only result in thrombocytopenia, but they have also been found either to inhibit or activate platelets. Inhibition by antibodies of the function of different receptors on platelets, such as collagen receptors, the glycoprotein (GP) Ib/IX (acquired Bernard-Soulier syndrome) or the GPIIb/IIIa complex (acquired Glanzmann's thrombasthenia), results in a haemorrhagic disorder very similar to the situation where the respective receptors are absent. On the other hand, reports have described a number of antibodies that activate platelets. The mechanism by which they do so varies and can involve interaction with the Fc receptor present on platelets, activation of the complement system or direct activation by binding to a signal-transducing antigen. Although the presence of such antibodies is expected to aggravate the problems due to the frequently occurring immune thrombocytopenia, treatment of these patients essentially relies on classical immunosuppressive therapy. In the case of activating antibodies, antithrombotic measures, such as anticoagulants or antiplatelet agents, can be envisaged.