“…This ADCC activity is still dependent on CD16 (FcgRIIIa) on the NK cells, as shown by Fab 2 anti-CD16 blocking and enhanced ADCC of ghPR1A3 over uhPR1A3 in the presence of enriched NK cells. The improved ADCC activity of the glycoengineered antibody is achieved without affecting PR1A3's binding activity, leaving it membrane specific, as described earlier (Durbin et al, 1994;Stewart et al, 1999). This is an important property of PR1A3, given the finding that soluble CEA can accumulate in lymph nodes and lead to false positive detection of cancers in lymph nodes when using other anti-CEA antibodies for immunoscintigraphy (Granowska et al, 1989).…”