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monoclonal Abs against tumor-expressed target Ags offer the possibility to re system to combat malignant tumor growth (1). The cruit the innate immune cellular arm of innate immunity comprises immune effector cells,such as monocytes/macrophages, polymorphonuclear cells (PMNs),and NK cells, whereas the complement system constitutes an integral part of the humoral arm (2). Cellular attack mechanisms are triggered by Abs’ Fc regions through interaction with FcRs, expressed on immune effector cells, to mediate Ab-dependent cellmediated cytotoxicity (ADCC) or Ab-dependent cell-mediated phagocytosis.Fixation of the C1q component of the classical complement pathway to target Ag-bound Fc is typically required to induce complement-dependent cytotoxicity (CDC) against target cells |
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