Read: That's the cancer I cured single handedly during coffee break.
OK, I'm busted
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The real history of this is much more interesting and embarrassing. The molecular targets of these antibodies, proteins called PD-1 and PD-L1 (Programmed Death-1 and Programmed Death Ligand-1) were known about in the 1990s. PD-1 is a protein on the surface of T and B lymphocytes, cells that are responsible for the immune response. PD-L1 is a protein on other cells of the immune system called antigen-presenting cells and macrophages.
Certain types of immune lymphocytes, killer T cells, directly kill cells that are detected as foreign, such as cells infected by disease viruses. B cells secrete large amounts of antibodies, which are more useful to fight bacterial infections. Other types of T cells, called regulatory T cells, are responsible for both ramping up an immune response and shutting down the immune response once it's no longer needed. Together PD-1 and PD-L1 signal immune T and B cells to stop dividing and to actually die off.
In most fields of molecular biology, the ramping up mechanisms are much more interesting and sexy than the mechanisms that shut things down. Both are critically important. It's just like in Star Trek when the Self Destruct Mechanism is activated – nobody really likes those Self Destruct systems.
By the early 2000's this PD-1/PDL-1 programmed cell death signalling mechanism was recognized. The cancer research world ignored it for years until it became known that some tumor types acquired the ability to express large amounts of PD-L1 protein. They could escape an immune response by fooling the killer T cells to ignore them and die off instead of rapidly dividing, invading the tumor, and killing it. Its like, Alec Guiness (Obi Wan Kenobi in Star Wars) who fooled the Imperial Storm Troopers by saying "these are not the droids you're looking for".
It had been known for years that tumors somehow caused the immune system to be unresponsive, but no one understood how this worked. By 2008-09, it was understood that covering up a T or B cell's PD-1 protein with an antibody could block PD-1/PD-L1 signalling, and prevent this unresponsiveness. By 2014 the first positive results were reported in patients with melanoma. Clinical trials in other types of cancer soon followed.
It took the cancer world two decades to catch up with the rest of molecular biology and immunology
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