So many things going on I forgot to add. This was a group effort, and the other person deserves more of the credit than I do. The person wants to remain anonymous.
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This post ties well with my Paradoxical Acquired Immune Dysfunction hypothesis, PAID part II - The Toll of TLRs and all Plagued by Design one, two , The Case for Reverse Mareks, A Stronger Case for Reverse Marek and It´s (viral) Evolution baby I recommend you to read it.
First, before we go any further, the reader needs to understand a basic aspect of immunology and your immune system. At a very basic level:
Th1 cells stimulate cellular immune response, participate in the inhibition of macrophage activation and stimulate B cells to produce IgM, IgG1. Th2 stimulates humoral immune response, promotes B cell proliferation and induces antibody production.
Your immune system is usually in a homeostatic state, and after being presented with “parts” of a foreign cell, it will secrete (produce) cytokine, small proteins that serve multiple functions, and as a signal, after enough cytokine is produced, it will go into Th1 or Th2. Allergic reactions are a Th2 response, Th1 is more inflammatory.
This is called the immune shift. Another aspect is immune skew, which is a term more used to refer to CD cells. Here is how it works. The mRNA vaccines cause a massive CD4 skew, refer to my other articles to understand why it’s bad.
Link to the article of the image and caption below.
In that first image, in my Reverse AIDS hypothesis, you can see the mRNA vaccine causes a strong skew both towards CD4 (you need that for a vaccine, it’s an antigen (foreign cell) response, and to Th1. You can find many recent papers discussing this Th1 response. Messing with TLR will also skew your immune system towards what I will describe below.
Besides everything else already covered by other scientific writers, that entails two things. Those others didn’t. A Type II Interferon response, meaning the sole member of its family, Interferon-γ (gamma). And Interleukin-12. IL-12 has its own family of cytokines. IL-12, IL-23, IL-27, and IL-35, but also belong to the IL-6 superfamily.
IL-12 and IFN-γ both belong to the same axis, Macrophages (they will pick up part of foreign cells and present to lymph nodes, to your immune system), will secret IL-12, which puts you into a Th1 state, which secretes Interferon--γ , which in turn makes you produce more IL-12.
Defects in the interferon-gamma and interleukin-12 pathways
The IFN-gamma/IL-12 pathway is central in immune control of both environmental and autochthonous challenges, as reflected in human mutations and animal models. Besides being crucial for mycobacterial control, the IFN-gamma/IL-12 pathway is also involved in the pathogenesis of autoimmune disease as well as tumor development and control. Genotype-phenotype correlations have been established for certain genes in this pathway, some of which have therapeutic implications.
Innate and adaptive immune defects associated with lower SARS-CoV-2 BNT162b2 mRNA vaccine response in elderly people
being integrin-β7 a maker of cell homing to gut. It is remarkable, that the decrease in integrin-β7+ CD1c+ mDCs was correlated with a higher IFN-γ production by TEMRA CD4+ and CD8+ T cells in response to SARS-CoV-2 two months after vaccination
Early on, you do want a broad (CD4/CD8) immune response, and a higher level of IL-12.
My TLR post is very important, and here is an addition, that shows TLR 7 can induce IL-12 and shift you towards Th1.
Interferon-α and Interleukin-12 Are Induced Differentially by Toll-like Receptor 7 Ligands in Human Blood Dendritic Cell Subsets
These immunogenic Th1 responses are mediated by IL-12 and IFN-α/β from MDCs and PDCs, respectively (22, 29). In line with this paradigm of Th1 responses, this study shows that TLR-7 signaling affects both DC subsets so that they support the differentiation of naive Th cells also toward Th1 cells, depending on the cytokines each DC subset secretes
T-Cell Hyperactivation and Paralysis in Severe COVID-19 Infection Revealed by Single-Cell Analysis
Collectively, CD4+ T-cells from severe COVID-19 patients are hyperactivated and FOXP3-mediated negative feedback mechanisms are impaired in the lung, which may promote immunopathology. Therefore, our study proposes a new model of T-cell hyperactivation and paralysis that drives immunopathology in severe COVID-19.
My argument by posting all these papers, and the graph above is not that the vaccine or breakthrough infections are paralyzing or even exhausting the immune system, but causing a transient dysfunction, and a consequence of suck imbalance is creating a biochemical loop and feeding and accelerating pathology (disease). And this is one part of the pathway.
These are the genes Interleukin-12 can up and down-regulate.
BolA family member 2 enhances cell proliferation and predicts a poor prognosis in hepatocellular carcinoma with tumor hemorrhage
BOLA2 mRNA expression is significantly higher in HCC tumour tissue than in nontumour tissue. Furthermore, loss-of-function studies determined that BOLA2 plays critical roles in promoting iron overload, tumor growth and TH.
These are some of the genes on the list. Here is what they do, feel free to go down this abyss.
When upregulated:
PSME2 - Renal Cancer, plasma cell myeloma
PDCD4 - Alzheimer’s Disease, prevents cell death
MTAP - Liver, lung, and prostate cancer
CA1 - Subacute thyroiditis, rheumatoid arthritis, human ischemic diabetic cardiomyopathy
GSTA2 - Liver cancer, Parkinson’s disease, leukemia
RALA - liver cancer, pancreatic cancer, lung cancer, breast cancer
CNN2/Calponin 2 - Gastric cancer, Atherosclerosis
CFL1/Cofflin 1 - Gastric cancer, lung cancer, pancreatic cancer, Alzheimer's
Downregulated:
ANXA2/Annexin A2 - Muscular Dystrophy, prostate cancer, cardiovascular disease
SOD2 - Hepatic cancer, cervical cancer, urological cancer, when expressed with ANXA2, esophageal squamous cell carcinoma.
Down-regulation of placental Cdc42 and Rac1 links mTORC2 inhibition to decreased trophoblast amino acid transport in human intrauterine growth restriction
This is but one of the mechanisms of the vaccine, and breakthrough infections, due to impaired and dysfunctional immunity, will set off, cause, and accelerate many diseases. But wait, there is more.
Increased levels of serum interleukin-12 in Graves' disease
Increased levels of serum interleukin-12 in patients with autoimmune thyroid disease
Go back to Reverse AIDS, I left a huge clue. The Epstein Barr paper. Without CD8 response, you can’t fight cancer or chronic infections, and you get the reactivation of many diseases. One of the biggest drivers of thyroid diseases is EBV. Corona is a coinfection and chronic best friend.
Possible involvement of IL-12 expression by Epstein-Barr virus in Sjögren syndrome
There are two things I left for last. First, a specific protein and gene mentioned in that image. PPIA. Also known as Cyclophilin A.
Cyclophilin A and CD147: novel therapeutic targets for the treatment of COVID-19
Inhibition of SARS-CoV-2 Infection by the Cyclophilin Inhibitor Alisporivir
Cyclophilin A Inhibitor: Potential Therapeutics for the Treatment of COVID-19
Cyclophilin A: a novel biomarker for cardiovascular disease in patients with type 2 diabetes
An annotation I have here. I could go on, for literally hours, about CypA, and its important role in all of this, but I think I made my point.
" Oxidative stress and inflammation play key roles in the development of pulmonary arterial hypertension (PAH). Cyclophilin A (CypA) is secreted in response to oxidative stress and promotes inflammation and cardiovascular disease. Endothelial cell (EC) dysfunction is an early event in the pathogenesis of PAH."
CypA also influences Liver fibrosis, cardiovascular diseases, viral infections, neurodegeneration, cancer, rheumatoid arthritis, sepsis, asthma, periodontitis, and aging. Among others.
The second thing is among the most significant one. Tyk 2.
The image of both is a good way to learn about TYK/JAK pathway. Why is that important ?
Diabetes, the TYK2 Gene and the Interferon Response: In Search for Environmental Causes
TYK2, a Candidate Gene for Type 1 Diabetes, Modulates Apoptosis and the Innate Immune Response in Human Pancreatic β-Cells
Our observations collectively reveal a novel role of STAT3 in Aβ-induced neuronal death and suggest the potential involvement of Tyk2/STAT3 signaling in AD pathophysiology.
TYK2: An Upstream Kinase of STATs in Cancer
Dysregulated TYK2 activation, aberrant TYK2 protein levels, and gain-of-function (GOF) TYK2 mutations are found in various cancers.
Potent and Selective Knockdown of Tyrosine Kinase 2 by Antisense Oligonucleotides
In agreement with the depletion of TYK2 proteins, several TYK2-mediated cytokine signaling pathways, including IFN-α and IL-12, were inhibited upon ASO treatment. Our results established the TYK2 ASOs as investigational tool compound and potential therapeutic agent for the treatment of autoimmune diseases and severe COVID-19.
Large amounts of IL-12 for too long, or at the wrong time of infection, will modulate certain genes and produce either too much or too few specific proteins. Which in turn can feed diseases under specific states.
Which in turn will lead to the expression of other cytokines, leading to more expression of TYK2, which basically is creating a cascade. This is merely ONE part of the pathway, we passed the middle.
To recapitulate, the mRNA vaccine obliterates your CD8 for weeks, which in turn skews your entire immune system to a specific dominant state, while hindering your ability to fight chronic infections, certain diseases, and cancer. By this skew, it might set off whatever your genetic lineage is weak towards, plus any reactivation of your latent infections will feed off to this pathway, which we gave a name.
All these posts were an over-simplification, but most will be able to get the idea of it. The next post will get severely worse FYI.
And I ask the reader again. Give what you have read so far in all my SARS-CoV-2 posts.
Are breakthrough infections harmless ? Do you still believe that ?
In the end, all roads lead to Rome…
We have two pandemics running in parallel: Sars-Cov-2 whose genome includes Uracil, and an isomeric version of Sars-Cov-2 used in the cmRNA vaccines, coded with Pseudouridine. All spike proteins created by body (In response to the cmRNA vaccines) will be isomeric. So will the antibodies. ICU cases of Covid-19 are caused by two lethal antibodies: REGN10987 and B38. This, then, is the mechanism of the cmRNA (chemically modified RNA or modRNA) vaccines: a huge quantitiy of isomeric abs are being produced, while the immune system can no longer fabricate the same number of regular (normal) abs as before, including the two lethal abs mentioned above. But now, the vaccinated people have a huge number of isomeric abs (including the lethal isomeric versions) in their bodies, which are awaiting an activation. Spike proteins = T-bacilli discovered by Wilhelm Reich a long time ago. Spike proteins = prions = T-bacilli. These prions can become misfolded (dextrorotatory) during a time of stress, a thermal shock (volcanic eruptions), or using biological scalar weapons. It is now well known that there are neurotoxic misfolded antibodies as well. The T-bacilli cause hypoxia and thus clotting.
I had considered for some time if this was a bio-weapon and what property would you give it.
Imagine if you would a virus that when people are in small groups causes no issues. The moment you add population density, you trigger the ability to infect and kill. The Antarctica event was interesting as based on their methodology they should have carried no virus into that isolated area. Instead, what if the vaccinated can produce "Covid19" by mere proximity to each other?
That'd be one heck of a virus, you'd decimate groups of people.. so cities, military, etc. Any group that gathered would self infect and self destroy itself, in theory. This matters more after the booster, when your immune system is gone.
So vaccinated hospital staff with sick vaccinated patients, if the above is correct, becomes a death sentence.
Interesting.