Member Info for RayPointer

Briefly going back to moditope.
The cd4 cytotoxic cell, in addition to retaining all the properties of the general , it also has cytotoxicity.
Does this sound about right?

So our cd4 general can
1) activate the innate immune system
2) talk to b cells thus facilitating antibody production
3) aid in a CD8 attack of the pathogen

Seems like a useful fellow to have around in a fight.

So having a strong cd4 memory may be a key factor.

So people with a weaker innate system have to rely more on the adaptive immune system.
Having strong memory both in B cells and T Cells may give the best chance.
So, yet another question. In the case of an antibody based vaccine, to what extent do the B cells and Cd4 cells talk to each other to form a broader response? Will the antibody based vaccine also result in memory T cells and maybe, more importantly, what level of avidity do these cells have.
As Lindy said, it is not easy.

And it may be that in healthy individuals the innate immune system just gobbles up the intruders without resort to the adaptive immune system. This might be what happens in asymptomatic individuals.

So that in turn leads to another question.
How long does the memory effect of the B Cells last?
Another question is how well do the adaptive and innate immune systems work together during a Covid19 attack?

Would a vaccine that gives a boost to both branches of the immune system potentially give the best results?

https://www.geo.tv/latest/294340-new-study-suggests-antibody-levels-in-recovered-coronavirus-patients-decline-quickly

It occurs to me that what is missing is a graph of antibody level of patients over time showing how the antibody levels vary pre, during and after recovering from an attack of covid19. Such a study may be impossible to produce.
What I am attempting to say that it may be hard to gauge the significance of recording antibody levels of 1.8 and 2.8 times when compared to recovered patients.

How long do high antibody levels last?

Don't look at the date of the article I posted LOL.
Another glass of wine is called for.

Perhaps a Freudian slip.

It always seems to me that Lindy's science is ahead.
The article I posted stated that cytotoxic CD4 TCells could be the next big thing and Lindy announced Moditope back in 2012.
Do these guys not read?
Having said that, it is always good to see people catching up with what Lindy has already discovered, even if they are thinking their work is ground breaking.

Ruck
Only generous ones I trust

Ruck
I could do with a nephew like that.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1809194/

Conclusion

"The role of CD4+ T-cells in immunity is complex as exemplified by their multiple functions. Evidence now shows that CD4+ CTL exist in vivo in humans, which challenges our ordinary view of CD4+ helper T-cells in contrast to CD8+ killer T-cells. What their role and its importance is in the immune response remain totally unclear. Nonetheless, the study of CD4+ T-cell subsets of differentiation and the identification of analogous CD4+ CTL in the mouse should provide the means to get some answers. When the existence of suppressor CD4+ T-cells was first reported, much skepticism was raised; 10 years later, these cells raise the strongest interest. Is the same fate awaiting cytotoxic CD4+ T-cells? The answer is yet to come."

No references to Lindy's work on Moditope.

So why look for a plan B?

But Inan has posted an article stating that targeting citrullinated epitopes could by a way of attacking certain viruses.
We know that the route of stress->autophagy->citrullinated epitopes is present in both auto-immune diseases and cancer.
Why not in viruses as well? These are cells in a hostile environment. It sounds to me that it is quite plausible that the same sequence exists in other types of cells.

We have already seen that immunobody is versatile enough for Lindy to use it in a Covid19 vaccine.

Isn't is becoming increasingly apparent that the combination of well chosen targets and high avidity TCells could be used to treat a diverse range of diseases?

But moditope goes a step further in that it activates the CD4+ cytotoxic TCell. This is a cell that Lindy herself describes as "absolutely amazing". This could turn out to be a pivotal discovery of a type of CD4 T Cell that contradicts the normally accepted role of the CD4 TCell as a helper to CD8 TCells.

Probably Lindy wouldn't be interested in moditope for viruses at this stage. It would be too much of a distraction.
But if a pharma were to buy moditope they might very well expand the scope, certainly as far as extending the patents.

"As such, it is likely that immune recognition of citrullinated epitopes also plays a role in pathogen clearance. Indeed, our recent data suggest that responses to citrullinated peptides facilitate recognition of novel influenza strains. Therefore, increased understanding of responses to citrullinated epitopes may provide important insights about the initiation of autoimmunity and recognition of heterologous viruses."

Well Karolinska Institut certainly started getting interested in moditope because of the link with autoimmune diseases such as RA.
Now we hear the cirtullinated epitopes may be targets for influenza strains and possibly other viruses.

Scope creep?

England certainly need a plan B

That was included in my list of questions.
Well perhaps the SP at 5p is ludicrously high in that eventuality.

The point I was making is that,we all hope the SP will at some point be based on the increasingly proven IP of the science.
Exponential SP rises would be nice.

You simply cannot predict the point at which big pharma wake up to deciding that Scancell's IP is potentially huge.

Will it be on a successful SCIB1 combo trial?
Will it be on great initial Modi1 results?
Will if be on a very effective Covid19 vaccine?
Will it be on a Biontech deal?
Will it be on an Avidimab deal?
Will they never wake up? (on the interest of balance)

The price is 5p because the price is being set by market buys and sells.
One day, we hope, it will be big pharma setting the price.