“…Thus, efforts have been made to optimize MoAbs by isolating switch variants using cellular [ 1 1,121 or molecular [13,14] techniques. For instance, the comparison of human chimeric IgGl, IgG2, IgG3, and IgG4 antibody effector functions showed that the chimeric IgGl was much more effective than all the other IgG subclasses in mediating ADCC using human FcyRIf effector cells, as well as in complement-dependent hemolysis 1141 Similarly, the functional analysis of mouse isotype-switch variants, isolated from an IgG 1 -secreting hybridoma, showed that tumor lysis was optimum when the IgG2a switch variant was used, while IgGl and IgG2b were virtually inactive [17]. In fact, mouse IgG2a and human IgG1 are of particular interest in ADCC, since they strongly bind FcyRI which is an excellent cytotoxic trigger molecule, notably when expressed on interferon y (1FNy)-treated cells [5].…”