Institute for Immunology, University of Erlangen-Nuremberg, Glückstr. 4a, 91054 Erlangen, Germany

Correspondence to: M Herrmann, Institute for Immunology, University of Erlangen-Nuremberg, 91054 Erlangen, Germany. Tel: +49-9131-85-36345; Fax: +49-9131-35776; E-mail: martin.herrmann@med3.imed.uni-erlangen.de

^†Edited by A Rosen

The phagocytosis of dying cells is an integral feature of apoptosis and necrosis. There are many receptors involved in recognition of dying cells, however, the molecular mechanisms of the scavenging process remain elusive. The activation by necrotic cells of complement is well established, however, the importance of complement in the scavenging process of apoptotic cells was just recently described. Here we report that the complement components C3 and C4 immediately bound to necrotic cells. The binding of complement was much higher for lymphocytes compared to granulocytes. In case of apoptotic cell death complement binding was a rather late event, which in lymphocytes was preceded by secondary necrosis. Taken together complement binding is an immediate early feature of necrosis and a rather late event during apoptotic cell death. We conclude that complement may serve as an opsonin for fragments of apoptotic cells that have escaped regular scavenging mechanisms. Cell Death and Differentiation (2001) 8, 327-334

Complement binding; apoptosis; necrosis

AS, fresh autologous serum; AxV, annexin V; DiO₆C(3), fluorescent dye 3,3'-dihexyloxacarbocyanine iodide; FITC, fluorescein isothiocyanate; FSC, forward scatter; IS, heat inactivated autologous serum; NGH, nuclear granularity and hypochromicity; PBL, peripheral blood lymphocytes; PI, propidium iodide; PMN, polymorphonuclear cells; PS, phosphatidylserine; SSC, side scatter; _m, mitochondrial membrane potential; UVB, ultraviolet B light