For the immune system, passive memory is evident within days. Active memory is evident within weeks, with IgGs developing within 2 months.
That's not slow given the median survival numbers that are talked about. The "slow" explanation is often invoked for cancer immunotherapies, largely by companies that have immunotherapies that don't elicit effective immune responses.
I'm not really sure how this provides a means for the cell to "escape" apoptosis. PS is flipped to the outer leaflet during apoptosis, at which point it is recognized by phagocytes directly (see ref). So if a cancer cell is exposing PS on the outer leaflet, it is doing the exact opposite of disguising itself... it is in fact putting out a very specific signal for phagocytes to come and engulf it. So the disguise angle makes little sense. If anything, the antibody binding the phosphatidylserine would help disguise the cell from the phagocytes.
I would also expect that if this anti-PS antibody was really working, you'd expect bleeding as a mechanistic side effect in patients. Activated platelets expose phosphatidylserine to accelerate clotting (see ref). If anything, the antibody would inhibit this acceleration and decrease the efficiency of clotting.
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