NorthWest Biotherapeutics Inc (NWBO)

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You're right, it is a terrible explanation of what dendritic cells are and how DCVax-L is made on his part - because he wants to make it sound as ineffectual as possible.

So according to Adam, you "expose" the immune cells to the tumor. What's that supposed to even mean? That you mixed them up in a blender?

And then he trivializes the process even more by stating it's then "supposed" to find the tumor and kill it... implying, of course, that it won't.

Of course, he forgets to add GM-CSF and IL-4 into this "exposure", which helps serve to mature the DCs and also give them their additional "killing" potential.

So it's obvious he knows nothing at all about the actual process, and he's not going to take one second to try and understand it. Dr. O'Rourke told him it won't work, and that CAR-Ts will, and that's enough for Adam. No one ever shared with Adam that,

Upon activation, DCs are crucial inducers of T cell immunity and are therefore at the frontline of immune-regulated responses.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3858649/

Really, one might conclude that keeping Adam in the dark (knowing he won't do any real research himself) is in the best interests of those who feed him whatever nonsense they want him to spew to help further whatever case they are trying make or cause they want to facilitate.

As you and I well remember, this was the same guy that told us in the comments of one his articles that "the multi-antigen approach is DCVax's weakness because none of the immune responses are strong enough. The vaccine is spread too thin." What? And remember this one... "DCVax-L is like hitting a rhinoceros with birdshot." This was when he called NWBO's past trial data "unreliable" and that no one "believes those OS results would ever hold up in a larger, more rigorously conducted trials." And that "CLDX has done a much better job developing rindo than NWBO has with DCVax." And then he cites the past data that CLDX presented for Rindo as being the reliable data, stating, "No one is claiming rindo will be effective against all brain tumors, just those over-expressing EGVRvIII. The data presented to data support the single antigen approach for this subset of patients."

And we all know how that prediction turned out.

The primary purpose of a dendritic cell is to present the antigens from the tumor to the cells that actually do the killing. The dendritic cells aren't typically the ones that kill the cancer. Instead, their job is to get the cells that do actually kill the cancer (t-cells, natural killer cells, b-cells [the ones that the current CAR-ts kill off] and the rest of the army) to the tumor so those cells can kill it.

Dendritic cells are antigen presenting cells (APCs). Any quick review of the literature out there would have told him that. But he can't be bothered with actually researching and covering the facts of how dendritic cells might actually work, as he can't be bothered with representing the actual facts about anything related to the NWBO and its dendritic cell vaccines.

From this 2013 abstract,

It soon became clear that DC are endowed with the unique ability to function as professional antigen presenting cells (APC) critical for the development of adaptive immunity.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3694804/

However, if you can mature the DCs, they can also do some killing. There are dendritic cells that actually do have the ability to also kill the tumor themselves - they can acquire a cytotoxic component that allows them to do some actual tumor cell killing, and theses have been referred to as "killer DC (KDC)". Studies show that when you culture the DC with granulocyte macrophage colony stimulating factor (GM-CSF) and interleukin IL-4 (both of which are added to DCVax-L), as I mentioned before, I believe you can get the DCs to actually do some of their own tumor cell killing.

Recent studies have lent support to the notion that, besides their role as potent inducers and controllers of immune responses, DC may also be endowed with a direct tumoricidal function. This less conventional characteristic of DC has however received limited attention and has raised many questions as it relates to the actual ontology of so-called “killer DC”, the acquisition of their cytotoxic activity and the underlying mechanism(s) of tumor cell killing. We here review these aspects, further discuss the influence of DC tumoricidal potential on their APC function and their ability to promote or inhibit anti-cancer immunity. We speculate on the integration of this non-traditional property into the broad concept of cancer immunoediting. Possible options to harness and implement DC tumor killing activity in cancer immunotherapeutic strategies are evaluated.

DC endowed with cytotoxic activity have commonly been referred to as “killer DC” (KDC) although these cells do not constitute a separate, dedicated subset. Rather, multiple heterogeneous subpopulations, naturally occurring in vivo (native) or generated in vitro from specific precursors have been described. A similar degree of diversity and plasticity has been observed as it relates to the modalities of induction of KDC cytotoxic function and to the effector mechanisms underlying tumor cell killing.

Multiple studies have further documented that DC generated in vitro, essentially from bone marrow cells cultured with GM-CSF and IL-4, can exhibit tumoricidal activity, but considerably variable results were obtained in terms of cytotoxic mechanisms.

Something else that I found mentioned in a separate article is that dendritic cells are also the most efficient of all the immune cells at recognizing the "non-self" antigens.

While most innate immune cells (professional presenters) and certain cells of epithelial lineage (non-professional presenters) are capable of presenting antigens to the adaptive immune cells be it to varying degrees; yet the sentinel antigen-presenting cells (APCs) of the immune system are the DCs. DCs are the guardian APCs because they are both efficient at antigen-presenting and adaptive immune cell activation and also good at judging whether an entity possesses “self” or “non-self” antigens. The ability of DCs to present “non-self” TAAs properly to prime as well as to activate adaptive immune cells is an absolute pre-requisite for activation of potent anticancer immunity).

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3858649/