Role of complement in immune or idiopathic thrombocytopenic purpura.

Abstract

The clinical course of immune or idiopathic thrombocytopenic purpura (ITP) is variable, suggesting different mechanisms for the decreased platelet count. The complement factors C3 and C4 have been detected on platelets, both alone and in association with immunoglobulin G (IgG), and a reduced platelet survival time has been described. Platelets have the capacity to interact with the complement system since they have both complement receptors and complement regulatory proteins on their cell membranes. The membrane attack complex (C5b-9) induced by antiplatelet antibodies generates platelet microparticles in a concentration-dependent manner. A marked variation in resistance to this phenomenon has been demonstrated between individuals and between men and women. These platelet microparticles seem to retain their biological role in haemostasis. Platelets also appear to play a role in the processing of immune complexes. Immunoglobulins and complement factors are found in several clinical situations where circulating immune complexes are expected. Furthermore, human platelets bind immune complexes in vitro and the reaction can be blocked by antireceptor antibodies to immunoglobulins and complement. These findings raise a number of questions about the role of complement in the pathophysiology of ITP.