Blood platelets have antigenic determinants on their surface, which can induce the formation of antibodies causing autoimmune thrombocytopenia (AITP). These autoantibodies are in most cases directed against epitopes on the glycoprotein complexes IIb/IIIa, Ib/IX and/or V. The determination of the relevant antibodies is necessary for the diagnosis of AITP. An example, how autoantibodies can directly cause death of target cells, is by activation of the complement system via the classical pathway, where immune complex formation on the cell surface ultimately leads to cell lysis. Another possibility - at least in some patients - might be the direct targeting of complement regulatory proteins of the cell membrane by specific autoantibodies. Two prominent examples of such regulatory factors are CD55 or decay accelerating factor (DAF) and CD59 or membrane inhibitor of reactive lysis (MIRL). They are also present on the surface of blood platelets and are therefore potential targets for autoantibodies in AITP. However, the presence of such antibodies has not been systematically investigated to date. An involvement of the complement system in AITP pathogenesis is of specific interest particularly with respect to recently developed therapeutic strategies. In the present study, we investigated the presence of autoantibodies against complement regulatory factors CD55 and CD59 in serum, as well as autologous platelets, of patients with AITP.