Member Info for RayPointer

Ruck I would say the one in 2013 was on behalf of Nottingham University. After all Scancell had to do a deal with NU to take over the development. I am just guessing now, but maybe Lindy's cohorts of PHD students will have done more work on glycans under Lindy's direction since 2013.

If the past is anything to go by, Lindy's science is always ahead of what she says in presentations. Is she waiting for the GC results before starting work on Modi3? IMO I would say no. Has work been done on the glycan platform. IMO, I would say yes. She works on something until she is happy to apply for a patent, and then she talks about it.

So the autophagy and presentation of the peptides are post entry of CD4 into tumour. A truly remarkable process end to end. I know Lindy says moditope was an accedental discovery. I think if you are as talented, knowledgeable and dedicated as Lindy obviously is, then discoveries happen

Thanks crumbs. I think I will call it a night now

Has the autophagy already taken place when the CD4 cell enters the tumour. Alternatively, does the sequence of events starting with the IFNs cause the autophagy?
Or could it be either?

No wonder she smiles!

It really is mind boggling how Lindy has completed such a difficult jigsaw puzzle. I, for one, need another wet afternoon to understand this part of the process LOL

So just for this part of the process 1 Activated CD4 cell enters tumour 2 IFNs are released 3 IFNs are taken up by nearby APCS 4 MHC is upregulated on the APC 5 the APC releases chemokines 6 the chemokines help to inflame the tumour more Making it an even better target

You are fast approaching 33333 posts C7 I will toast you when that moment arrives ATB

And 6 perhaps

And so there is further APC involvement in the actual killing

Right, so the last part of 5 thru to 7 is the actual killing process.

I was under the impression that once the tcells Are activated that is the end of APC involvement

And 6

The tcells need to be activated ( as opposed to being naive) and there needs to be enough of them to mount a worthwhile attack. So activation and clonal expansion are 2 of the key factors.

Exactly, but it is a natural immune system process. The trick is to cause the activation of Tcells having a particular TCR. Even that is a natural process once you have got the right molecules or part molecules ingested in the APC.

Then if the memory cells already exist why does the cancer establish itself? As part of clonal expansion of the tcells, some become long living memory cells.

I think you will find that Lindy's Moditope mouse experiments exhibit a memory response

Clonal expansion is an important process that the immune system uses to mount an effective attack.

Both moditope and immunobody cause the production of memory T cells as well as the killer variety. This is something that happens naturally either as the TCells are activated or close to the tumour. Checkpoint inhibitors, on the other hand, do not cause production of memory TCells.