Macrophage-mediated tumoricidal activity generated by human C-reactive protein (CRP) encapsulated in liposomes is complement-dependent1
Savita Gautam, Ph.D.
Karen James, Ph.D.
Sharad D. Deodhar, M.D., Ph.D.
Human C-reactive protein (CRP) incorporated into multilamellar vesicles (CRP-MLV) has been shown to activate peritoneal exudate cells (PECs) to inhibit tumors. This activity is comparable to that of another macrophage-activating agent, liposomal muramyl-tripeptide (MTP-MLV). The present study shows that the complement system is involved in the CRP-MLV-induced tumoricidal response. Normal mice were depleted of complement and treated with CRP-MLV or MTP-MLV. PECs were later harvested and mixed with T241 tumor cells. After incubation, this mixture was injected into the footpads of normal mice. Sacrificed animals were evaluated for tumor growth and lung metastases. These were significantly inhibited in mice injected with T241 tumor cells mixed with PECs from donors treated with CRP-MLV, but this antitumor activity was lost in mice that received a mixture of tumor cells and PECs from donors depleted of complement before the treatment. Complement depletion, however, had no effect on the antitumor activity of MTP-MLV-induced PECs.