The mechanics of antibody-dependent enhancement

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I'm no immunofag, and only stumbled upon this ADE thing when looking for more info on SARS-CoV-2 vaccine on some articles on Nature that for some reason Hiro thinks aren't cool enough to not be considered spam. I'll try to link them in a later post.
As I've understood, the complement antibodies have binding sites for certain receptors on phagocytes, so that when they bind to a pathogen they also mark it for the phagocytes to, well, literally eat it up. I also understand that virus, too, bind to receptors on cells to infect them by injecting genetic materials and machineries into the cell, so I've always assumed that phagocytes have something to prevent this from happening with the "complemented" pathogen they're going to eat, and activating phagocytosis instead.
Apparently not, or at least not always. But I still assume that in most cases it wouldn't happen, and the phagocytes would just do the usual business of swallowing up the pathogen. What's bothering me is, what decides which one of the two possibilities occur instead of the other?