Polytrauma is characterized as a syndrome of multiple injuries with defined severity which leads to a massive systemic immune activation and to secondary dysfunction and failure of remote, initially uninjured, organs [1, [5] [6] [7] . Clinical studies have demonstrated that complement activation occurs in plasma of patients after major trauma, as early as at the time of presentation in the emergency department [169] [170] [171] . The extent of complement-mediated inflammation was correlated with injury severity, tissue hypoperfusion, and posttraumatic [171, 172] . Serum levels of C3 and C3a were identified as markers of injury severity and outcome in multiply injured patients [173, 174] . Moreover, expression profiles of complement regulatory molecules and of the anaphylatoxin C5a receptor (C5aR/CD88) appeared to be significantly altered in leukocytes of multiply injured patients during the early phase of polytrauma, compared to blood samples from healthy volunteers [175] . The expression profiles of CD46 (membrane cofactor protein; MCP), CD59, and C5aR (CD88) on neutrophils correlated inversely with the severity of injury, an observation which was attributed to an intriguing trauma-induced "complementopathy" in multiply injured patients [175] .