Great question, and one I've asked myself. The answer lies within PS specific receptors, and it's a RAGE, so to speak... Here's a better way to ask your question, "does immunogenicity of apoptotic cells increase by masking PS?" To answer that question, one must understand PS receptor functionality. For example, there are PS specific receptors of phagocytes, that are purposefully initiated for anti-inflammatory signalling. One can build a model of physiologic immune effect from here, without me going deeply into teach mode.
The point being that, a response is initiated as demanded, which is activated from specific PS receptors.. When a patient is dosed with chemotherapeutic agents, a specific demand is created. It's localized at a pathogenic site, and a PS specific receptor is initiated. Here we would have created a dockable immunosuppressive PS molecule for Bavituximab.
Do you have any answers, or only questions? No disrespect intended, just think if you can ask hard question, you might be capable of answering tough questions...
Physiologically speaking what are some of Phosphatidylserine's a multi-functional purposes? How are these functions initiated? Answer these questions for the board please... I've already given you one, and a clue for others..
All the best,
John
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