I might be misunderstanding this, but it looks like humans would either:
Suppress T-cells and B-cells that react against transposase at the negative selection step during maturation, making vaccination impossible
Already be immune to the antigen (maybe that would be possible if the transposon is expressed very rarely, otherwise it would be recipe for auto-immune damage)
Full disclosure: I’ve forgotten everything about immunology since ~5 minutes after my last immunology exam.
The fact that we have a lot of autoimmune disorders suggests that the negative selection step isn’t perfect.
If you want to vaccinate I think you would start with a peptide that’s not identical to a transporase subjection but similar and first give a vaccination dose against that. Then you vaccinate again with a peptide that’s more similar and work your way towards transpoase.
Reading more it’s likely that PGBD5 actually gets used productive in the brain to increase cell diversity and thus isn’t as good of a target.
PGBD5 being upregulated in Alzheimers and in brain tumors makes the PGBD5 Alzheimers link interesting. If PGBD5 gets constantly expressed in train cells and creates a lot of DNA damage, it’s plausible that this leads down the line to enough mutations to be a problem and Alzheimers appearing.
Edit: somehow I mistook the link to be about Alzheimers because that’s what a googled for. It’s instead about sporadic Creutzfeldt-Jakob disease. I however have found another study that does make the link https://doi.org/10.1371%2Fjournal.pmed.1002487
Having been able to predict that link between Alzheimers and PGBD5 ahead of time seems interesting.