Written By: Alana Karran
The first annual Community Symposium on the Molecular Basis of ME/CFS was held at Stanford University on August 12th, 2017. Sponsored by the Open Medicine Foundation, the Symposium featured talks by the world’s leading experts in ME/CFS research and related fields that are informing that research.
Immunologist Mark Davis, PhD, spoke on the ever-present question of autoimmunity in ME/CFS. To understand where the current research is headed, Dr. Davis first explained how the immune system works and how autoimmunity is determined.
The immune system is made up of white blood cells that patrol the body looking for invaders like bacteria, viruses, parasites, etc. When these pathogens are detected, the immune system utilizes cytokines – small proteins that are important in cell signaling – to communicate with each other and coordinate a defense.
The innate immune system acts quickly by creating inflammation to immediately populate the area of urgent need with white blood cells to fight off a pathogen. The Adaptive immune system responds later with very specific receptors, like B cells, T cells and NK cells. The body makes every possible receptor/antibody at the gene level, ahead of time, to assure it can formulate a targeted attack on pathogens, such as viruses, that replicate much quicker than the immune system.
Once a T or B cell is a match for a particular pathogen, it signals cell division or “clones” itself to respond to only the intruder it has detected. Sometimes, the immune system makes a mistake. It may start out producing a response to a virus, for example, but if the proteins or peptides – degraded proteins – in that virus are similar to something in your body, like your heart or another organ, it will begin attacking that organ instead. This is what is known as autoimmunity.
In a study of cytokines in ME/CFS patients, done by Dr. Jose Montoya at Stanford, 17 of the 51 cytokines in the body were consistently elevated, correlating with severity of symptoms. These particular cytokines were related to inflammation and indicate a systemic response by the innate immune system.
In another study, conducted by PhD Candidate Marvin Gee and Dr. Christopher Garcia at Stanford, evidence of clonal expansion in T cell receptor sequences were found in ME/CFS patients. This indicates an active adaptive immune system response. In particular, there is evidence of CD8+ T cell involvement, also seen in MS, Lyme and Cancer. This suggests there is an autoimmune component to ME/CFS.
Because every T and B cell holds the original memory of its pre-programmed immune response, researchers can trace back these cells to the virus, bacteria or parasite it matches. So far, they have been able to isolate one particular T cell receptor in ME/CFS patients. The next step is to determine what pathogen matches that response.
This research may help discover what pathogen initially triggered ME/CFS. It may also help identify if that pathogen has similar peptides to an organ or system in the body, indicating an autoimmune response.
In summary, according to Dr. Davis, the conclusions from the various research so far into inflammation and immune response in ME/CFS are as follows:
Elevated cytokine levels, correlating with severity of symptoms in ME/CFS patients, indicate a strong inflammatory component.
There is evidence of CD8+ T cell involvement, and likely other types of T cells, suggesting an autoimmune disease.
Research into the specific activated T cells is ongoing and may locate the initial pathogen as well as the tissues being attacked by the body.
“There’s been a great deal of controversy and confusion surrounding ME/CFS — even whether it is an actual disease. Our findings show clearly that it’s an inflammatory disease and provide a solid basis for a diagnostic blood test.” ~ Mark Davis, PhD