Multiple Sclerosis after mRNA Vaccine (Mechanism)
Another Spike-ey treat!
The video:
Multiple Sclerosis after mRNA Vaccine (Mechanism Discussion)
The paper , “Covid-19 Vaccination can induce Multiple Sclerosis via cross reactive CD-4+ TCells recognizing Sars-CoV-2 spike protein and myelin peptides” (# 0942) is from a group of researchers at University Hospital in Zurich, who are careful to declare the safety and efficacy of the MRNA vaccines while at the same time saying, in essence, that the presence of spike protein can in some people lead to the development of autoimmune disease that may be temporary or longer lasting. (TBD)
The study looks at two cases of MS developed in close temporal relationship to mRNA vaccination.
The study set out to find out if the onset of MS in these two cases was caused by CD4 T-cell clones…copies of the T cells…that cross recognize SARS-CoV-2 spike protein derived peptides, and peptides derived from the myelin proteins that look similar to myelin sheath pieces previously implicated in multiple sclerosis.
I will explain, but first ….What is MS?
To quote the Mayo Clinic:
Multiple sclerosis (MS) is a potentially disabling disease of the brain (CNS) and spinal cord .
In MS, the immune system attacks the protective sheath (myelin) that covers nerve fibers and causes communication problems between your brain and the rest of your body. Eventually, the disease can cause permanent damage or deterioration of the nerve fibers.
Signs and symptoms of MS vary widely between patients and depend on the location and severity of nerve fiber damage in the central nervous system. Some people with severe MS may lose the ability to walk independently or ambulate at all. Other individuals may experience long periods of remission without any new symptoms depending on the type of MS they have.
There's no cure for multiple sclerosis. However, there are treatments to help speed the recovery from attacks, modify the course of the disease and manage symptoms.
How does the spike trigger MS?
Neurons are encased in a myelin sheath that ensures that nerve conduction runs smoothly.
A neuron has a cell body that has many small branches called dendrites. Other neurons send signals through the dendrites. Dendrites are the receivers of those signals.
The Neurons have a long branch called an axon through which it sends outgoing signals.
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The axons are wrapped in fat or lipid rich cells called the myelin sheath. The myelin sheath enables the nerve transmission impulse to travel from one node to another faster than it would if the myelin sheath was not present. Simply put, if the myelin sheath is damaged, nerve conduction becomes disrupted, travels through the neuron very slowly and gets out of sync with the rest of the nervous system
In the presence of a myelin sheath, nerve transmission happens smoothly from node to node. These nodes are called Nodes of Ravier.
Schwann cells create an insulating layer around the axons of the peripheral nervous system.
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In the peripheral nervous system, the myelin sheath is made by Schwann cells which wrap themselves around the axon like a ring layer by layer.
In the brain, or central nervous system, the myelination is made by a different kind of cell, called oligodendrocyte.
Although the functional outcome is the same it is important to keep these two cell proteins in mind as they are referred to in the study.
Oligodendrocytes make the myelin sheath for brain axons
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Another background concept to keep in mind relates to the proteins present in the myelin wrapping of the neurons, both schwann and oligodendrocyte.
MBP, PLP and MOG are proteins, not cartoon characters!
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MBP (myelin basic protein) and PLP( proteolipid protein) are found inside the myelin sheath, and on the surface of the myelin sheath is another protein called MOG (myelin oligodendrocyte glycoproteins). These proteins are often targeted by our immune system. When the cytotoxic T-cell antibodies attack these proteins it causes local inflammation and destroys the myelin cells, denuding the axon and disrupting the nervous system’s function. It can become quite disruptive, even life-threatening.
Here’s how it can happen…
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A dendritic cell chops up an antigen and presents the pieces to activate the adaptive arm of the immune system .
The innate arm of the immune system picks up an antigen…it could be spike protein from either the virus or the vaccine… it will chop it up into smaller pieces and then present those pieces on its surface to the MHC2 molecule . Then the T helper (CD4) cells from the adaptive arm of the immune system will bind there and if it recognizes this antigen, will become activated.
So far so good?
Here’s the key point …
The piece of the spike protein looks in its composition very similar to MOG protein found on the myelin sheath. The immune system becomes sensitized to the spike and the macrophages or dendritic cells pick it up. They present it on their surfaces and now there are CD4 cells that become sensitized to it and they become active.
Activated CD4 can make antibodies via two pathways:
In the presence of Interleukin 4 and 6, and absence of interleukin 12, the naive T helper cell becomes T helper 2 cell which in turn releases interleukin 4, interleukin 5, 10, 13 and so on, which help modulate the immune system and cause the B cells, which are antibody making cells, to convert into plasma cells which are actually active B cells that will now be making antibodies.
If the T-Cell has a binding region that could bind with the part of the spike protein that looks very similar to the MOG protein, then the antibodies produced will also go and bind to the MOG.oops!
That is the autoimmune response.
2. It is also possible that the naive T cell instead of having interleukin 4 actually has interleukin 12 secreted on it and there is no interleukin 4 plus there is interferon Alpha and that will cause this CD4 cell to become a T helper 1 cell. T helper 1 cell in turn releases interleukin 2 and causes the cytotoxic T cell or CD8 positive cell to become active. The activated CD8+ cell will have a similar binding site as the helper cell and now this CD8+ cell will then go and try to crush and destroy the spikes but at the same time it would also start cross reacting with the myelin sheath cells and destroy them in the process. T helper 1 cell in turn produces interferon gamma which will then go and act on the macrophages and dendritic cells and further amplify the process.
Why doesn’t this happen to everybody? Because everybody ‘s bodies are different and it is unfortunate that some of us have a binding protein in the myelin sheath that can be mistaken by the activated immune system as an alien that needs to be taken out.
Now for the study…
The researchers took peripheral blood and cerebrospinal fluid samples from two cases who developed Multiple Sclerosis in close temporal association with the MRNA vaccine. They wanted to know first if they had T Cells attacking the spike protein, and secondly if the T Cells that are attacking the spike are also attacking the myelin sheath.
They Put CD4 Cells into a culture with spike protein pieces, and isolated those cells that were reactive to the spike protein. Then they took those reactive cells and made copies of them and put them in another dish with the myelin sheath protein pieces , PLP, MVP and MOG.
How did the researchers figure out if they were active against the Myelin proteins?
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Remember, when the T helper 1 cells become active they release interferon gamma. So after a period of incubation they found interferon gamma in the supernatant.
To double check they took the reactive cells, made copies of them and tried it again with the same results. Here was the proof that the activated TCells were cross reacting to spike from the vaccine and myelin sheath cells.
Self-reactive T cells were detected from Spike specific T cell populations in both patients. CD4+ T from CSF also showed reactivity to MBP, MOG, PLP peptide pools. Finally, we found proinflammatory T cell clones that recognize both Spike protein and immunodominant MBP peptides and MOG peptides, which have previously been implicated in MS.”
Concluding that:
“…the onset of MS in these two cases is very likely caused by CD4+ T cell clones that cross-recognize SARS-CoV-2 S protein-derived peptides and peptides derived from myelin proteins, which have previously been implicated in MS.”
Postscript
There had been a theory in the past that maybe immune cells have two binding sites but this theory has since been discarded, and it is now accepted that T-cell helper or cytotoxic B cells have only one binding site.
So the question is: What is the mechanism that leads to this cross reaction, where it never did before the spike came in? How does that self-tolerance break down?
https://www.youtube.com/live/UmDOMfMjcLM?feature=share
Here are two videos from DrBeen.com that will shed light on this issue:
Self Tolerance and Microbe Triggered Autoimmunity (B Cell Focus)
Self Tolerance and Microbe Triggered Autoimmunity (T Cell Focus)