Almost all cell types can recognize, respond to, and ingest apoptotic cells by using specific sets of phagocytic receptors that bind to specific ligands on apoptotic cells. Detailed genetic studies in Drosophila and Caenorhabditis elegans have recently yielded evidence that basic phagocytic mechanisms and pathways for the recognition and engulfment of apoptotic cells are highly conserved throughout phylogeny [7,8]. In vertebrates, a number of receptors have been identified that can mediate phagocytosis of apoptotic cells. These include, for example, scavenger receptors and pattern recognition receptors such as CD36, SR-A and CD14, integrins such as the vitronectin receptor αvβ3, and members of the collectin family and their receptors CD91 and calreticulin [9-13]. The individual roles of these molecules in binding, phagocytosis or transduction of anti-inflammatory signals upon apoptotic cell recognition have not been well defined, however [5,6,14]. The importance of efficient mechanisms for apoptotic cell clearance in vivo is supported by the observation that autoimmune responses can be provoked in mice when key molecules for apoptotic cell recognition and uptake are missing. This has been reported for knockout mice lacking the complement protein C1q [15], for mice with a mutation in the tyrosine kinase receptor gene Mer [16] and, more recently, in mice lacking transglutaminase 2 or milk fat globule epidermal growth factor 8 (MFG-E8) [17,18].