The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
The first place where this happened was in a class of medicines called checkpoint inhibitors. ... PD1, CTLA4 are some targets where there are drugs that are infused that hit these things that are on the surface of TE-C cells and they actually are natural breaks to the TE- cells. ... if you make a drug that hits the break on the on the tea cells, the tea cells go stronger and they can be unleashed against cancer just by taking the brakes off of them.
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Bookmarking — the dossier-vs-overview split is the right call. Most of the time I want overview; sometimes I want receipts.
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one of the Inhibitors are molecules on the cell surface on the surface of a of a lymphocyst will inhibit a surface now many more that when targeted by an antibody will not kill the cell but actually turn off the breakes that are keeping that cell's activity from exhibiting itself so it's releasing the brakes and it turns out to have a very important function in the body
um but the idea now was what about doing the exact opposite approach instead of trying to throw more uh fire at the te- cell what if we can take its breaks down less gas pardon me instead of giving more gas let's give less breaks
would giving people anti ca4 I.E taking the brakes off their immune system