Bless!
In understanding cancer immunity, it's essential to understand cytokines, which serve as a form of molecular lingua franca for our immune cells and the rest of our body to communicate.
Like any language it can be used for collaborative communication, as well as for exploitative manipulation. Furthermore, communication can break down, and the meaning of signals can change with context and exposure duration. Inflammatory signals are in this way exceedingly similar to human languages.
The English word ‘get’, for example can have up to thirty-three distinct meanings, depending on context. Likewise, if you hear the same word again and again and again, you shall invariably experience what’s known as semantic saturation, where the word loses all meaning to you and becomes meaningless noise.^1^
Your cells interact the same way with inflammatory signals as do our brains with language. Where our natural languages have words (technically morphemes, but this isn’t a linguistic dissertation) as the smallest unit of meaning, our inflammatory ‘language’ has cytokines (a molecule used to send cell-to-cell signals) as its smallest units of meaning. Cells can ‘listen’ to cytokines by having the appropriate receptor (a molecule used to receive cell-to-cell signals) to detect it. If a cell doesn’t exhibit the receptor for a certain cytokine, then it can’t hear whatever signal is encoded by that given cytokine.
Similarly to words in natural languages, each cytokine can have a plethora of meanings in various contexts and can change or lose its meaning, when repeated too often for too long. This is the simplest and most intuitive mental model I’ve found, when trying to understand inflammation, inflammatory signalling, and the cytokines involved therein.
To understand how cytokines can influence the behaviour of our immune system, we must know, that our immune system has primarily two functional domains it needs to balance constantly. On the one hand, it needs to destroy pathogenic invaders, infected cells, and defective ones before they turn into cancerous ones. On the other hand, it needs to repair tissues damaged by infections, injuries, or by its own destructive half.
This balance is achieved by having some immune cells be able to re-polarise from destroy-type to repair-type behaviour, by having other immune cells, which are inherently destroy-type or repair-type, and by having another layer of immune cells, which act as regulators of and intermediators between the former two.
As this is a whole subject of biology unto itself, we shan’t discuss it deeply here.
Just know, that our immune system can operate in a mode of destruction, a mode of repair, and any interpolation between the two, and that our immune system constantly monitors itself and communicates with the rest of the body in order to remain balanced and beneficial to the body as a whole.
Speaking of communication.
This is where cancer cells and their nefarious manipulation of the immune system comes in. The perhaps most studied cytokine in all of tumour biology is the membrane-bound programmed death ligand 1 (PD-L1), which is readily expressed by cancer cells and repair-type immune cells.^2–5^ PD-L1 binds to a receptor on the surface of destroy-type T cells and disallows them to execute their ordinary cell-killing function. It’s far from the only cytokine used in this way by cancer cells, nor is it the only result cancer cells use cytokines for.
There are many other cytokines, which can be used by cancer to manipulate the immune system to its benefit, but which also can be used by us to manipulate the immune system to the detriment of cancer.
By re-polarising the immune system from a tumour-supportive repair-type state to a tumour-exterminating destroy-type state, we can effectively use the same manipulation of the immune system, which cancer uses, just to achieve the exact opposite result, namely the healing of your body of cancer.
This is one of the many tools our Mosaic Method tries to use in healing you.
In the upcoming booklet on the Mosaic Method, this will feature heavily. Until then, I hope this has been interesting.
God speed,
Merlin L. Marquard
P.S.: For more on immune manipulation against cancer, you may check out the articles:
- On Ganoderma Mushrooms and Cancer Immunotherapy,
- On the Alleviation of Persistent Spike-Protein Pathology,
- Helping Cancer Heal through pH Neutralisation,
- On the Complexity of Nitric Oxide in Cancer and the Prospect of Hydrogenated Water over Methylene Blue,
- On The Therapeutic Potential of Tocilizumab in IL-6-Positive Cancers, or
- Anecdotal Success in Using a Soft Pharmaceutical Regimen to Lower the IL-6 Status in a Patient with Malignant Pleural Mesothelioma.
References
- Zhang X, Lian J, Yu Z, et al. Revealing the mechanisms of semantic satiation with deep learning models. Commun Biol 2024;7:487. doi:10.1038/s42003-024-06162-0
- Karwacz K, Bricogne C, MacDonald D, et al. PD‐L1 co‐stimulation contributes to ligand‐induced T cell receptor down‐modulation on CD8+ T cells. EMBO Molecular Medicine 2011;3:581–92. doi:10.1002/emmm.201100165
- Sheppard K-A, Fitz LJ, Lee JM, et al. PD-1 inhibits T-cell receptor induced phosphorylation of the ZAP70/CD3ζ signalosome and downstream signaling to PKCθ. FEBS Letters 2004;574:37–41. doi:10.1016/j.febslet.2004.07.083
- Sprooten J, Vanmeerbeek I, Datsi A, et al. Lymph node and tumor-associated PD-L1+ macrophages antagonize dendritic cell vaccines by suppressing CD8+ T cells. CR Med 2024;5. doi:10.1016/j.xcrm.2023.101377
- Velcheti V, Schalper KA, Carvajal DE, et al. Programmed death ligand-1 expression in non-small cell lung cancer. Laboratory Investigation 2014;94:107–16. doi:10.1038/labinvest.2013.130
