Therefore, we analyzed the contribution of C3- and C5-dependent complement activities in a mouse model of N. meningitidis sepsis after intraperitoneal (i.p.)infection by comparing wild-type (WT) mice with C3−/− mice (completely devoid of complement effector functions) and Hc°/° mice lacking C5 (allowing C3b opsonization but devoid of MAC and C5a formation). This evidence concerns the gene C5AR1 and infection.