HOST defence and inflammatory responses are controlled and amplified by receptor-mediated events often initiated by a chemotactic factor that directs the approach of phagocytic cells¹. Complement receptors CR1 and CR3 are responsible for the phagocytic and adhesive properties of neutrophils ^2,3, whereas the C5a receptor mediates the pro-inflammatory and chemotactic actions of the complement anaphylatoxin CSa^4–6. In addition to stimulating chemotaxis, granule enzyme release and superoxide anion production, this receptor stimulates upregulation of expression and activity of the adhesion molecule MAC-1, and of CR1, and a decrease in cell-surface glycoprotein 1 GOMEL-14 on neutrophils^7–9. In vivo, the C5a receptor may participate in anaphylactoid and septic shock ^10–12. The human C5a receptor was cloned from U937 and HL-60 cells and identified by high affinity binding when expressed in COS-7 cells. The deduced amino-acid sequence of the receptor reveals the expected motifs befitting its interaction with cellular GTP-binding proteins.