Why some suffered (and died) with severe C-19 whilst others were fine?
And vitamins and supplements that may help balance your immune system.
A THREAD 🧵
Before we delve into how we improve our immunity, we must know what we are working with.
Today’s focus is T cells, and there are various types.
It all starts with Th cells.
Naive T helper (Th) cells are T cells that have no role.
But when presented pathogenic material by other cells and an interaction is formed using certain receptors Th cells into “effector Th” cells, also known as CD4+ cells.
These effector Th cells are further divided into three main types, identified by the cytokines they secrete.
Cytokines are small secreted proteins released by cells that have a specific effect on cell interactions and communication.
The three effector Th cells are referred to as Th type-1 (Th1), Th type-2 (Th2), or Th type-17 (Th17) cells.
Th1 cells secrete the cytokines interferon (IFN)-γ, and tumour necrosis factor (TNF)-β. This makes it easier for these cells to fight infections caused by viruses, bacteria, and other microorganisms that grow inside macrophages (another type of white blood cell)
Th2 cells secrete another type of cytokine called interleukins, specifically IL-4, IL-5, IL-10, and IL-13, which up-regulate antibody production and target parasitic organisms and allergens.
Th17 was later discovered and shown to secrete IL-17, IL-17F, IL-6, IL-22, and TNF-α, and it appears to play an important role in tissue inflammation as well as neutrophil activation to combat bacteria existing outside cells.
In broad terms, Th1 cells work best against viral infections, Th2 cells work best against parasites, and Th17 cells work best against bacterial and fungal infections.
Th1, Th2, and Th17 populations and the cytokines they release are antagonistic to each other, meaning that they work in opposition.
And so during an infection, one predominant type of effector Th takes control, depending on the pathogen.
There is another form of T cell that can be formed around this time called regulatory T (Treg) cells.
They secrete IL-10 and transforming growth factor (TGF)-β, which modulates helper T cell activity and suppresses some of their functions. They are thought to maintain tolerance to self-antigens, and help prevent autoimmune disease.
I hope you can appreciate that the immune system relies on certain cells doing their job properly and communicating with other cells in the correct way.
But, asynchronicity causes chaos, and, for some, death.
It has been noted that those who suffered with SEVERE COVID-19 had:
- “a significant reduction of %Th1 and %Th17 cells with higher activated %Th2 cells in the COVID-19 patients compared with reference population.”
Before you carry on, if you’d like a more detailed summary of immunological differences between COVID-19 severity and what you may be able to do about it, then it’s all in one place, the book 👇🏾
So as well as other immunological differences (not mentioned here), those who suffered SEVERE C-19 had less Th1 than Th2 and Th17; and T reg cells tended to be lower in those with severe COVID-19 too.
Whilst those who had MILD or non-hospitalised COVID-19 tended to have greater Th1 and better T reg activation.
Overall, it looks like the bodies of people who had severe COVID-19 responded to the virus as if it were a parasite instead of a virus.
And because the predominance of one Th cell reduces the evolution of others, their disease took off like a runaway train. This train only got faster and more out of control due to a lack of or dysfunction of its braking system: T reg cells.
Unfortunately, in those who died, their immune system became so exhausted that it ceased to work at all, as noted here: “Senescent Th2 cell percentage was an independent risk factor for death accompanied by the numbers of total lymphocytes”
Don't only focus on C-19; it has long been known that patients infected with HIV who show a Th1 response are seronegative (antibody negative) and do not develop AIDS, whereas Th2 patients become seropositive and evolve to AIDS.
Balance needs to be kept for the immune system to work well, and there is more and more evidence that these mRNA agents greatly upset this balance.
But how? 👇🏾
Stress less.
Cortisol is colloquially known as the "stress hormone," but its relationship with our immune system is less appreciated. Cortisol has been shown to shift T-helper status from Th1 to Th2 dominance.
One study noted sleep restriction in humans caused an unfavourable shift in the Th1/Th2 cytokine balance towards Th2 activity that was strongest during the daytime.
Research has shown that polysaccharides from I. obliquus affected the Th1/Th2 lymphocyte ratio and Th17/Treg in the colon and therefore could possibly treat inflammatory bowel disease.
Melatonin has shown the ability to influence the differentiation and trafficking of immune cells, to activate Th1 lymphocytes, and to enhance NK activity.
Methylene Blue, a drug with a colourful history and wide-range of health benefits including improving mitochondrial efficiency, anti-viral, neuroprotection, and anti-ageing.
A THREAD 🧵
Methylene blue (MB) has a colourful history, having been the first synthetic drug used in medicine as well as being used as a dye in the textile industry.
In medicine, it was used to treat malaria more than one century ago, as well as being one of the first drugs used to treat patients with psychosis at the end of the 19th century.
Its discovery led to the development of other antimalarials and antipsychotics.
With an estimated incubation period of 5 to 40 years, and health care workers currently not making the link between any jabs and jab-related illnesses. The prevelance of prion diseases might be low...for now.
Imagining tripping in the centre of London with your dad and siblings in 1799 😂
A time when Prime Minister William Pitt the Younger introduces an income tax of two shillings to the pound to raise funds for Great Britain's war effort in the French Revolutionary Wars.