What if immune tolerance wasn't a bug, but a feature?

“COVID vaccines “work” by instructing your immune system to give up the fight against the virus”

An important post on Rintrah.nl :

“COVID vaccines “work” by instructing your immune system to give up the fight against the virus”

revisits the issue of immune tolerance.

He starts with the common belief:

“Thanks to protections from being vaccinated & boosted, I’m grateful to only be experiencing mild symptoms.”

and then goes on to explain where it goes wrong.

“But this lie, this idea that a reduction in symptoms from a viral infection is an indicator the vaccine you received against it has worked, is so deceptive, so dishonest, so dangerous, that I feel morally obliged to explain why it’s wrong.”

Rintrah points out that the “vaccines” developed by Pfizer look effectively similar to a tolerance induction therapy developed by Pfizer at the same time.

The only difference is the lipid carrier used.

He writes in a linked post:

New-generation mRNA and adenovirus vectored vaccines against SARS-CoV-2 spike protein are endowed with immunogenic, inflammatory and immunomodulatory properties. Recently, BioNTech developed a noninflammatory tolerogenic mRNA vaccine (MOGm1Ψ) that induces in mice robust expansion of antigen-specific regulatory T (Treg) cells. The Pfizer/BioNTech BNT162b2 mRNA vaccine against SARS-CoV-2 is identical to MOGm1Ψ except for the lipid carrier, which differs for containing lipid nanoparticles rather than lipoplex. Here we report that vaccination with BNT162b2 led to an increase in the frequency and absolute count of CD4^posCD25^highCD127^low putative Treg cells; in sharp contrast, vaccination with the adenovirus-vectored ChAdOx1 nCoV-19 vaccine led to a significant decrease of CD4^posCD25^high cells. This pilot study is very preliminary, suffers from important limitations and, frustratingly, very hardly can be refined in Italy because of the >90% vaccination coverage. Thus, the provocative perspective that BNT162b2 and MOGm1Ψ may share the capacity to promote expansion of Treg cells deserves confirmatory studies in other settings.

The paper on this “tolerogenic vaccine” for the treatment of experimental autoimmune encephalomyelitis was released in January 2021.

So the induction of tolerance here, in the setting of treating autoimmune disease such as multiple sclerosis is a very desirable goal. The possibility of being able to treat autoimmune disease and chronic inflammation without inducing systematic immune suppression seems to be the promise of this knowledge.

This review from the journal Cellular Immunology, Sept 2020, is important I think.

https://www.sciencedirect.com/science/article/pii/S0008874920303336?via%3Dihub

These “FOXP3⁺ regulatory T cells (Tregs) constitute a critical barrier that enforces tolerance … to ensure tissue-specific resistance to autoimmune, allergic, and other inflammatory disorders”.

The paper explores how T Cell antigen Receptor (TCR) specificity and antigen recognition efficiency shape the Treg and conventional T cell (Tcon) repertoires to adaptively regulate T cell maintenance, tissue residency, phenotypic stability, and immune function in peripheral tissues.

It’s the tissue residency role that particularly caught my eye, given the autopsies of the covid jabbed who died unexpectedly had infiltrates of CD4 lymphocytes in the tissues such as the heart.

Back to Radagast’s article:

An important point:

A reduction in severe cases and death, can not be sufficient to consider a vaccine against this virus a success. The reason is because such a reduction can be achieved in a very simple manner: By simply not fighting the virus.

Further

We now know that if you destroy the adaptive immune system of mice, this does not make them more vulnerable to SARS2. No, it makes them experience zero symptoms. These mice are unable to eliminate the virus, although their innate immune system keeps the viral load stable. This fits data I have seen reported on MERS, where people with HIV just don’t suffer symptoms from the infection.

In addition, just because your body stopped fighting this virus, does not mean this virus stops harming you. This is a virus that infects the endothelium, the cells lining your blood vessels. So what does it look like, when your body doesn’t bother fighting a virus that infects these cells? You may feel fine, but then you suffer an unexpected heart attack or stroke. You died of COVID, but because the vaccine discouraged your immune system from fighting the virus, your death did not look like a COVID death.

So covid deaths in the covid jabbed, with an immune system which has given up the fight against the virus may simply look like an unexpected heart attack or stroke, or an unexpected clot.

Failure to achieve herd immunity against this virus, which is clearly damaging people’s brains and immune systems, is an existential threat.

Radagast makes the point that the viral load, the hospitalisations and high excess mortality in high vaxxed countries all look like what you expect to see, when a population’s immune response is no longer trying to fight this virus?

Finally, the article ends with:

The evidence we have suggests that virulence is merely increasing, with BA.2.86 representing a return to greater virulence, with a Delta-like Furin cleavage site that causes increased cell damage.

And it now seems to be going a step further, with a further improvement to the Furin cleavage site that has never been seen before

And that sounds disturbingly close to #GeertVandenBosschewasRight for my liking.