Re: prostate cancer and cell vaccines

A couple basic immunology points and a question:

"dendrite, (memory cells,)"

- dendritic cells aren't memory cells (only certain lymphocytes - T and B cells - have memory phenotypes). DCs are pretty long-lived, but they don't demonstrate "immunological memory" - a DC's secondary response to a given antigen is no different than a primary response.

"Even if dendritic cells can... find an antigen to copy"

- Dendritic cells do not "copy antigen": they phagocytize (basically, gulp in) antigen, process it into little peptide pieces, and then present those pieces on MHC molecules on their cell surfaces. The antigens presented by a dendritic cell are pieces of the actual pathogen (or tumor, or unaltered self cells), not copies.

"Even if dendritic cells can see through histocompatability molecules"

- dendritic cells don't "see through" MHC (major histocompatibility complex). Dendritic cells express MHC molecules (nothing special in expressing MHC-I, as just about all nucleated cells do this, but they also express MHC-II, which is what allows them to activate T-helper cells).
DCs present self-antigen (including tumor antigens) all the time - dendritic cells are like little scavengers, just gulping up whatever is around them and presenting whatever they find on their surface MHC molecules.
The problem isn't usually getting DCs to process and present tumor antigens - the problem is the fact that the DCs that do so are often unable to activate T-cells. Because dendritic cells present self-antigen all the time (they present way more self antigen than they present foreign antigen), T-cells won't just become activated because they see their specific antigens on a dendritic cell. The dendritic cell needs to "co-stimulate" the T-cell - it needs to give the T-cell a secondary signal, usually B7. In the absence of co-stimulation, T-cells become anergic - not only aren't they activated against the antigen at the time, but they become resistant to activation in the future. This is an important way that we maintain tolerance to our own tissues. Pathogens can activate dendritic cells to express co-stimulatory molecules, but self-tissues usually do not. The problem is that because tumor cells are "altered self", they look a whole lot more like our own healthy cells than they look like pathogens, so the dendritic cell that is presenting a tumor antigen is often not expressing co-stimulatory molecules and T-cells therefore aren't activated.

Histocompatibility molecules are not an impediment to dendritic cells processing and presenting self proteins.

"even if they can then transfer that code to killer lymphocytes"

Dendritic cells do not transfer code to "killer lymphocytes" (neither to CTLs nor to NK cells nor to NK T-cells, although I'm assuming that here you're talking about CTLs?) Before a T-cell is activated, it already has the "code" of the antigen it is capable of going after (because that's the antigen that, when complexed with MHC, is able to bind that particular T-cell's T-cell Receptor (TCR). T-cells are educated in the thymus and when they're done maturing and are exported to the periphery, they all have different TCRs, each one specific for a different antigen. That's the "code" that determines which antigen the T-cell will be able to go after).
Dendritic cells bring the antigen to the T-cells and activate them. T-cells become activated when they "see" (bind) an activated dendritic cell carrying the antigen that the T-cell is specific for. The T-cell binds the antigen/MHC complex on the dendritic cell's surface, and if the dendritic cell provides appropriate co-stimulation to the T-cell, it will be activated.

"Some of the most successful vaccines occurred after they gave chemotherapy. This means that chemo compound injured the cancer so much that it could not metabolically manufacture histocompatability molecules"

Again, you seem confused about the role of MHC. MHC molecules do not make it more difficult for the adaptive immune system to kill a tumor or intracellular pathogen. On the contrary! If virally infected cells or tumor cells do not express MHC-1, CTLs cannot recognize them as targets and kill them. This is why a lot of viruses and tumors try to evade the immune system by down-regulating MHC-1.
MHC molecules are essential to a T-cell response!


Question: You write that "tagging of antigen is bypassed" - I have no clue what you mean by "tagging". Do you know the scientific terminology of the phenomenon you are referring to, or can you otherwise explain in more detail what you're referring to (and preferably, provide a reference).

Thanks!

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