Gary, don't belittle DCVax's role as being a catalyst [original definition: "a substance that increases the rate of a chemical reaction without itself undergoing any permanent chemical change"] since DCVax plays the major role in the combination without which essentially nothing happens. Fill the patient up with a Checkpoint Inhibitor ("CI") (such as Keytruda/pemrolizumab) or an RNA Analogue (such as poly-ICLC) and the GBM carries on regardless. Treat the patient with DCVax-L and the GBM is attacked by T-cell lymphocytes to a greater or lesser extent. DCVax-L is the essential component without which nothing happens.
However, add the additional components of the triple therapy and you get more effect than that of the sum of its parts -
eg: Let's say that DCVax alone has x units of effect on GBM, pembrolizumab alone has y units of effect and poly-iclc alone has z units of effect.
If they all played an equal part then their combined action would be x + y + z units of effect.
Instead we find that their combined effect is something like 10x + y + z units of effect.
Without DCVax-L the others are as nothing. They are there purely to help DCVax do its job, the CI by suppressing the tumour's inhibitory environment and the RNA analogue by stimulating T-cell lymphocytes to greater activity. The CI and the RNA analogue are the catalysts which enable the DCVax-L sensitised T-cell lymphocytes to get on with their job unhindered and with a lot more oomph!