alex3619
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PS. Just thinking about all this, we have vasodilation and blood clotting? What in Hades does that combination do?
Welcome to Phoenix Rising!
Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of, and finding treatments for, complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia, long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.
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Makes us freakin' miserable.PS. Just thinking about all this, we have vasodilation and blood clotting? What in Hades does that combination do?
Makes us freakin' miserable.
The Role of Adaptive and Innate Immune Cells in Chronic Fatigue Syndrome/ Myalgic Encephalomyelitis
30 Fukuda diagnosed CFS patients and 25 controls were studied. Their disease duration was kind of short at over 2 years, which might imply (based on Lipkin's unpublished findings) that they were a CFS subgroup, the under 3 year group.
I was part of this study and have been sick 27 years, so I think they just mean at least 2 years
its not bad research eh!
whats next?
more depth with a bit of expansion with this and a higher cohort number........progress i feel.merry xmas everyone....no wonder we feel like shit!
im on my phone in a paddock i hope prof jonathan edwards has some comments.phone is difficult so i hope some kind person links this to his thread.
They are not specific about results, but alterations in platelets and sedimentation rates are implied to be increases in patients. So we might have an increased tendency to blood clotting and failure in microcirculation, which fits with much earlier findings in CFS of problems with blood flow and increased clotting that were treated with heparin.
Very helpful summary, thanks!
I wonder whether blood clotting is another issue where there are subgroups? My own erythrocyte sedimentation rate (ESR) has tested normal, and my blood seems to flow normally when I have a cut.
I have recently been getting to grips with some genetic test results from years ago, which I had filed away, and I have a variation in eNOS3 (endothelial nitric oxide synthase 3) that reduces platelet activity.
The Role of Adaptive and Innate Immune Cells in Chronic Fatigue Syndrome/ Myalgic Encephalomyelitis
An increase in memory cells might mean the body is fighting something. This implies pathogens or toxins, autoimmune or autoinflammatory processes.
This profile of B cells is consistent with an autoimmune disease.
Its more a propensity for blood clotting, to clot still requires secondary factors, and hence there will be some variability.
Just found that ESR is more about inflammation than blood clotting - need to refresh my memory before posting!
The Treg profile in this study was similar to previous find- ings (14, 64). The cause of heightened levels of Tregs in CFS/ME is unknown.
Surface expression of CD73 on CD4+ T cells was correlated with an increase in Tregs in the CFS/ ME patients. CD73 is an ectonucleotidase required for aden- osine production (65).
At optimal conditions, CD4+ T cells, in particular Tregs produce low levels of adenosine deami- nases (ADA), which breaks down adenosine (66).
High lev- els of CD73 with limited amounts of ADA enhance the levels of extracellular adenosine in circulation and this may accu- mulate in immune cells altering their functions (67).
On the cell surface of many leucocytes including Tregs, ADA binds to CD26 eliminating anti-inflammatory adenosine (66) and reducing suppression by Tregs.
Reduced levels of CD26 have been reported on lymphocytes in CFS/ME patients and this in conjunction with an increase in CD73 may increase Treg suppression in CFS/ME (68). Tregs may suppress NK cytotoxic activity and T helper cells via a number of path- ways including the generation of adenosine by CD39 and CD73 molecules (69, 70).
In the presence of adenosine, NK cells also produce high levels of IFN-γ (71). Extracellular adenosine has anti-inflammatory effects on both innate and adaptive immunes, specifically, it may dampen the activa- tion of Th1 and Th17 cells (72, 73).
Adenosine may also inhibit CD8+ T cell cytotoxic activity and the release of pro- inflammatory cytokines by CD4+ T cell subsets (74–76).
In mice, the presence of adenosine receptor agonist reduces NK cytotoxic activity due to a decrease in cyclic adenosine monophosphate (77).
In T cells, CD73 dampens the release of pro-inflammatory cytokines by inhibiting NFκB activation (78), promoting a Th2 type response.
High levels of adeno- sine or ATP activates a negative feedback process that inhibits neutrophil function and protects against prolonged inflammation or injury (79, 80).
In summary, the findings from this study confirm a sub- stantial breakdown in immune tolerance and inflammatory mechanisms in patients with CFS/ME. This likely involves significant impairments in the NK-cell function, over-reactive Tregs, impaired DCs, neutrophils, dysregulation in cytokine levels and abnormal production of adenosine.
Collectively, these defects are overwhelming and further confirmatory studies may be required owing to the multifactorial and het- erogeneous nature of the disorder. Importantly, it may be nec- essary to confirm the levels of circulating type I interferons in CFS/ME patients and the exact profile of memory B cells and immature B cells that are disproportional in CFS/ME.
Thank you!
Does anyone want the full text merged to that thread or shall I just delete mine?