Breakthrough Research Finds CFS is An Immune Condition
Australian scientists have linked chronic fatigue syndrome (CFS) to a genetic defect in immune cell receptors putting to rest once and for all the pathology of this much-maligned condition.
The research undertaken by the National Centre for Neuroimmunology and Emerging Diseases (Griffiths University) found that an inherited genetic defect means that cells do not work optimally.
These findings have potentially wider implications as many of the patients studied also had fibromyalgia and postural orthostatic tachycardia syndrome.
Mast-cell precursors have also been found in the blood of the patients studied. Whilst CFS patients might well fall under the spectrum of mast-cell activation, the Griffiths University research, by identifying the mechanism of action, provides a much more precise diagnosis.
CFS Genes Studied
Griffiths University is studying a pattern of single nucleotide polymorphisms (SNPs) in the TRP and acetylcholine receptors (AChM3R). If you have done a 23andMe test, you can use livewello.com, to extract the following indicative data.
Current CFS Research Findings
The receptors being studied by Griffiths University are not well researched. They are however known to act as part of a primitive “threat” sensing system.
Acetylcholine coordinates the brain’s response to environmental stimuli, either dialing up or dialing down, its response based on the level of perceived threat. It is also highly susceptible to acute psychological stress.
TRPA1 channels, for example, are cellular “threat” sensors that detect cellular oxidative stress and a range of stimuli both within and outside the cell.
It senses temperature, touch, pain, smoke, chemicals, solvents, mold, cold pain, and all manner of stimuli. It also appears to sense some medications.
Once TRPA1 channels are stimulated, TRPM3 moves calcium into the natural killer (NK) cell in order for it to work.
Griffiths University found that the TRPM3 receptors on natural killer (NK) cells are impaired with CFS. They fail to move calcium into the NK cell, which results in decreased cell function and specifically decreased cytotoxic killing ability.
Natural Killer Cells
Natural killer (NK) cells are cells belong to the innate immune system.
This is the part of the immune system that does not require previous exposure to certain types of threats in order to work. NK cells have a primitive ability to recognize stressed cells regardless of previous exposure.
NK cells can be divided into two categories and differentiated by the types of markers on them.
Cytokines – The first type is mainly capable of secreting cytokines, that act as mediators between different cells of the body, mainly cells of the immune system. They disrupt and contain the virus from spreading and facilitate the entry of the NK cells into the affected cell. This process is not necessarily impaired in CFS patients.
Cytotoxic Activity – The second type has cytotoxic activity, meaning that it can kill abnormal body cells, such as virus-infected, or cancerous cells. Griffiths University found that CFS patients have decreased cytotoxic activity of the NK cells.
Preferential Calcium Channel
Both TRPA1 and TRPM3 are parts of the preferential calcium channel which moves calcium into the cell to mount the NK cell’s defense.
Calcium is found in virtually every cell in the body and acts as a biological messenger responsible for carrying signals, through calcium channels, to target activities within cells. NK cells are no exception and require calcium to regulate their cellular functions.
TRPM3, however, has a secondary pathway distinct from the central pore that can be specifically activated by the combined application of Pregnenolone Sulfate and/or Clotrimazole, a drug used to treat yeast infections. Simplistically, this is a backup system, that can help move calcium into the channel when the primary pore is faulty.
What Does This Mean For CFS Patients?
The impact of altering a gene is not yet known. This is what Griffiths University are diligently working on together with the research into other SNPs that might affect overall function.
Whilst Griffith University believes it has found the primary mechanism of action for CFS there is much that needs to still be done to have a comprehensive solution. This includes screening methods.
If you are in Australia and have CFS then I would encourage you to consult with Professor Pete Smith.
My over-riding approach has been to remove the threats to my body (particularly mold, medications, stress, and dental issues), to create the optimal environment for healing (through lifestyle changes and targeted supplementation), and to support my immune system to calm down.
To a large extent, this has worked. I will always be vulnerable to CFS but the symptoms have gradually fallen away. I now consider myself symptom-free.
The articles cited in this article were read by an Associate Professor Of Immunology and summarized for me to ensure that the information above was technically correct.
Marshall-Gradisnik S, Smith P, Nilius B, Staines DR: Examination of Single Nucleotide Polymorphisms in Acetylcholine Receptors in Chronic Fatigue Syndrome Patients. Immunology and Immunogenetics Insights 2015, 7:7-20.
Marshall-Gradisnik SM, Smith P, Brenu EW, Nilius B, Ramos SB, Staines DR: Examination of Single Nucleotide Polymorphisms (SNPs) in Transient Receptor Potential (TRP) Ion Channels in Chronic Fatigue Syndrome Patients.Immunology and Immunogenetics Insights 2015, 7:1-6.
Nguyen T, Johnston S, Chacko A, Gibson D, Cepon J, Smith P, Staines D, Marshall-Gradisnik S: Novel characterization of mast cell phenotypes from peripheral blood mononuclear cells in chronic fatigue syndrome/myalgic encephalomyelitis patients. Asian Pacific journal of allergy and immunology 2016.
Huth TK, Brenu EW, Staines DR, Marshall-Gradisnik SM: Killer Cell Immunoglobulin-like Receptor Genotype and Haplotype Investigation of Natural Killer Cells from an Australian Population of Chronic Fatigue Syndrome/Myalgic Encephalomyelitis Patients. Gene Regulation and Systems Biology 2016, 10 :43-49.
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