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Therefore, our study has ldentified a previously unrecognized function for complement in tumor błology. We have shown that complement and NK cells interact and influence tumor growth by limiting tumor-specific CTL induction. Factors from the complement system may restrict NK celi availability in tumor tissue where NK cells would normally participate in the induction of a tumor-specific CTL response via, among other things, tumor celi lysis. Furthermore, complement proteins could also promote infiltration of the tumor by MDSCs that could then suppress lymphocyte function (Fig. 4D).

Many drugs targeting complement proteins are currently in clinical trials and few side effects have been reported (Kohl, 2006; Ricklin and Lambris, 2007). CVF has also been used