There's tons of this kind of work going on.
Are you trying to 'convince' yourself of something ? Are you brain-washed ?
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Everything works in theory.. see me things even work (to a degree) in practice.
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You can easily assess 'interest' though ..
Most of the successful scancell trials have been done over the past 2-3 years, including 2/3 deals.
The share price has lost 2/3 of its value....
Things move on. |
anyway that is why i feel i am capable of Assessing risk
because all the research is scancell focused on the stuff that actually matters the science |
so all this data gathering is ongoing ....
"this is what Big pharma want to see"
the nitty gritty .... stuff
total boring for investors
but its like Lindy Said at the dinner table nobody was interested in T cells and antibodies
until
Covid arrived
MRNA has managed to sell itself on that basis
but is it good enough for cancer without going down the highly expensive route of personal vaccines and even then does it work to the level to justify the cost to the mass market
I think its been over sold by the media ...An image imprinted of unproven capability |
Inan, "now if you still think i am an idiot ...."No, I've never said you are an idiot. |
one other thing Ruck ....
when you test for Avidity ... like what you posted they cultured the t cells
this is a early email with lindy
Re yes we did trial this kit but it could not read out avidity on our mouse T cells. In the human trial this is more difficult as we culture the T cells which can change their avidity. We have identified some specific TCRs from both SCOPE and Modify and we will now start measuring avidity.
Kind Regards,
lindy |
Immunobody ....
Goes DIRECT to APC
the mabs go only to the C64 on the APC that are involved in "inflammation"
and can control t cell function
to fight cancer
tick tock
It works |
the CD64 also controls which Dendritic cells to go after
Distinguishing marker:
CD64 expression can be used to differentiate between different types of dendritic cells, particularly helping to distinguish monocyte-derived dendritic cells from conventional dendritic cells.
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Pharmacological potentiation of monocyte-derived dendritic ...
Monocyte-derived dendritic cells (moDCs) are a type of antigen-presenting cell (APC) that can help the body's immune system fight cancer. They are a key component of anti-cancer DC vaccines, which are used to treat metastatic melanoma and other types of cancer. |
Scancell MAB's are controlling the
The Fc gamma receptor I (FcγRI or CD64) is the only human Fc receptor with a high affinity for monomeric IgG. It plays a crucial role in immunity, as it mediates cellular effector functions of antibodies including phagocytosis, antigen presentation, and cytokine production.
on Dendritic cells ..... |
so from all that ....
we know "High Avidity" works ....
Immunobody is proven
there is no other state that is higher ....
what Avidmab has done is given "second signal a boost by clustering"
its not one mab linking to the Dendritic cell its many and they hold hands via non covalent linking
its like having black paint v carbon nanotube black paint
go an look at the intensity !! |
now if you still think i am an idiot ....
what have the "non idiots posted" |
 one way to see if a vaccine function is to target direct like scancell and Krisma (ivy works for them) to the dendritic cell .....giving you control of the Avidity and type of cell function .... is if you see the word "Innate" which means they prime the innate which leads to adaptive which means the immune response is controlled by the immune system not the vaccine ...
which means you have to trick the dendritic cell with adjuvants
Krisma goes direct but adds adjuvants ...
Scancell goes direct and does not need adjuvants !!!
BioNtech
The architecture of our FixVac platform
Our FixVac (Fixed Vaccine) platform candidates consist of a fixed combination of mRNA-encoded non-mutated tumor antigens, which are known to frequently express within specific cancer types. The mRNA is formulated with our proprietary RNA-lipoplex delivery formulation which is designed to enhance mRNA stability in the body as well as to target antigen-presenting dendritic cells (DCs) – the boot camps of our immune system. By enhancing the ""presentation"" of these specific tumor antigens by DCs to the immune system, our FixVac candidates aim to trigger a strong and precise """innate""" and adaptive immune response against cancer cells expressing one or more of the respective tumor antigens. This approach offers the potential to also treat cancers with low mutational burden effectively, which represents half of all patients with metastatic melanoma. |
sorry Ruck its never a straight forward answer ............
if it was
Cancer vaccines would have been approved 20 years ago !! |
now in cancer "self Antigen" off the shelf vaccines
t cells Cannot see Self .................
so when looking at a target cancer cell it appears Normal ....
from Lindy
Its quite complicated but the reason we pick peptides rather that just use whole antigen is that if you use whole antigen the strongest peptide will bind to the appropriate HLA but for a self antigen the T cells to these peptides may be deleted to avoid autoimmunity. So the next best binder could stimulate T cells but is out competed by the stronger binder. If you just present the next best binder with no competition you get a great T cell response. We pick these next best binders from patients who have spontaneously rejected their tumour or who express the epitopes on their MHC AND make T cell responses to their tumour. The vaccine induces or boosts these responses.
Kind Regards,
lindy
Prof Lindy Durrant
CEO
Scancell Ltd
"next best binders" are weak ... so you need the High Avidity which respond to weak antigen |
so you have a natural selection of Low avidity T cells .....
normal vaccine against a virus No Problem those t cells will work fine
Cancer they will not ..........
you have to have High Avidity ....
so you are reversing the avidity from Low to High .....
that is why the vaccine is so clever
Scancells world |
most vaccine rely on your natural t cell repertoire
but High Avidity tend to be negatively selected "deleted"
High avidity in the thymus refers to the high level of interaction between a T cell receptor (TCR) and a self-peptide–MHC complex. This interaction occurs in the medulla of the thymus and leads to the deletion of self-reactive T cells.
Explanation
The thymus is a small gland in the lymphatic system that produces and trains T cells.
T cells are white blood cells that help the immune system fight infection and disease.
During development in the thymus, thymocytes undergo positive and negative selection.
During positive selection, thymocytes interact with cortical thymic epithelial cells (CTEC) and receive a survival signal.
During negative selection, thymocytes interact with medullary thymic epithelial cells (MTEC) or dendritic cells (DC) and undergo apoptosis if they are self-reactive.
The balance between tolerance and autoimmunity is determined by the regulation of T-cell avidity.
Autoreactive T cells can escape deletion by lowering their avidity.
When activated, these "tuned" T cells can cause autoimmunity. |
now if you keep attacking the cancer with these low avidity t cells that rarely kill
you can and will cause the cancer to effectively mutate in similar way as Bacteria become resistant to antibiotics
the cell loses the target antigen """Antigenic loss"""
Selective pressure
Cancer cells can lose surface antigens due to natural or therapy-induced selective pressure. These antigen-loss variants can cause therapy-resistant relapse.
Immunotherapy
Cancer cells can lose surface antigens due to immunotherapy, which can lead to therapy-resistant relapse.
so if you can kill the cell it cannot mutate ...
same as bacteria .... you have to kill them all
take the full course |
should work against cancer then .... however if you look at Biorix
you will see a peak of High avidity but its all the other low avidity t cells it induced as well
To test the functionality of identified clonotypes, 106 T cell receptors (TCR) from five epitope-specific repertoires were re-expressed and tested for peptide sensitivity. While recruited repertoires were overall enriched for high-avidity TCRs, differential clonal expansion was not linked to fine avidity differences. Instead, maintenance of polyclonality ensured robustness in counteracting mutational escape of epitopes. Our findings on the induction and maintenance of high-functionality polyclonal T cell repertoires shed light on T cell quality as a neglected criterion in the assessment of vaccine immunogenicity.
""shed light on T cell quality as a neglected criterion in the assessment of vaccine immunogenicity.""
so you probably didn't read your link correctly Ruck the issue is not that you will get some High Avidity ... as per biorix
it is the other clutter that is the issue
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"Differential clonal expansion was not linked to fine avidity differences"
means that while different T cell clones may expand to varying degrees during an immune response, these differences in expansion size were not directly correlated with small variations in their binding affinity (avidity) for the antigen, indicating that the immune system might prioritize other factors beyond just the highest avidity clones when selecting which clones to expand significantly.
for cancer you need ""specific clonal expansion of High Avidity T cells""
T cells will gain Avidity after an infection "battle hardened"
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Yes, T cells gain "avidity" during an infection, meaning their ability to recognize and bind to specific antigens presented by infected cells increases as the immune response progresses, effectively enhancing their effectiveness in fighting the pathogen; this process is often referred to as "avidity maturation" or "functional avidity maturation" where the T cells become more responsive to the antigen even without a change in the T cell receptor's inherent affinity.
so cancer primary issue ...
The T cells are not of a High enough Avidity and many vaccines induce a plethora of T cells of low Avidity
1/ problem many self antigens are weak antigens not a lot of them
so you need the High Avidity to see them To kill
2/ you have to get a foot hold to actually improve the t cells ability over time to increase Avidity
so you have Low Avidity t cells competing with High Avidity T cells
AI Overview
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Yes, a low avidity T cell can still "see" cancer, meaning it can recognize cancer cells and potentially interact with them, but it may not be as effective at killing them compared to a high avidity T cell; in some cases, research suggests low avidity T cells might even play a role in tumor control, especially when combined with other immune strategies like checkpoint blockade.
"""it may not be as effective at killing them compared to a high avidity T cell""" |
https://www.biorxiv.org/content/10.1101/2024.10.30.620795v1 |
https://bmjmedicine.bmj.com/content/2/1/e000468 |
mRNA vaccine high avidity T cells......mRNA vaccines, like those used for COVID-19, have been shown to induce high-avidity T cells. High-avidity T cells have a stronger binding affinity to their target antigens, which can enhance the immune response1. This means that the immune system can more effectively recognize and respond to the pathogen.Studies have found that mRNA vaccines generate robust T cell responses that are broad and long-lasting. These responses include polyclonal T cells, which are diverse and can target multiple epitopes on the virus, providing better protection against variants. Additionally, high-avidity T cells are less likely to be affected by mutations in the virus, making them crucial for long-term immunity1. |
You wouldn't know a time to 'buy' if it stared you in the face...lol |
I see Bitcoin is higher than when Trump announced tarifs ..lol |
Exactly as it should be in markets inane...
Think CONTRARIAN.
95% of investors will be wrong.
When popular opinion is one sided ....the truth is on the opposite side.
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That's how markets work.
Welcome to MY world... |
except ... i don't follow your propaganda
in fact there is nobody here that does |
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