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"It's been found immunological abnormalities and 2 biomarkers on CFS" Spanish National news paper

acer2000

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Thanks for posting this. Very interesting. I always have elevated CD4 cells. Doctors say this is common in virus infections (and some others), but they never can find one in me. Interesting also that they looked at CD57, most research on CFS (as opposed to Lyme) has focused on CD56. Maybe we will learn something new. EU29,000 seems like a relatively attainable goal as well.
 

lauluce

as long as you manage to stay alive, there's hope
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I speak spanish, their findings are very interesting indeed... hope this leads to a better diagnostic and treatment
 

Martial

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Interesting study, though I think these bio markers can become in one ways either connecting other chronic disease states; or possibly placing others in the category of CFS/M.E. as well

Mycoplasma infection, Bartonella, Certain herpe viruses, Mold, and many other infectious organisms all trigger the same response markers in the body, leading to inflammed cytokine responses in aforementioned immune system markers.

Dr. Shoemaker even made a recent study on the relation of auto immunity to T cell inflammatory conditions, hoping this would lead to possible curative treatment for many people diagnosed with auto immune disease.

http://www.survivingmold.com/

I was also reading recent work by Dr. Kleinhardt, and Dr Buhner who all mentioned similar findings.

Does this mean there is a common dysregulation, or infectious organisms in all these chronic disease states? It will be interesting to see what happens with that possibility.
 
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Yes, research shows that high NKp46 is associated with infections and anti-tumor activity (and possibly anti-liver damage) as well.

The question still remains as to whether these are specific biomarkers and that means comparing not to healthy controls, but cohorts of people with other illnesses and infections. (there are plenty of biomarkers for CFS, but none are highly specific).
 

serg1942

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Hola LAULACE, Encantado de saludar a alguien de habla hispana por aquí!;)

Does this mean there is a common dysregulation, or infectious organisms in all these chronic disease states? It will be interesting to see what happens with that possibility.
Hi MATIAL: Actually I am quite convinced that there're 3 theories that have tried to explain CFS, that actually suit for many other diseases:

1. For sure the partial block in the methylation cycle/low levels of GSH (Rich Konynenburg's theory based on Dr. Yasko's program) is one of them (We know how well it woks for autism, and how well it works for some PWCFS, especially when combined with treating the terrain, such as Lyme, or biotoxins). But it also works in Lupus and in MS, in my experience. Moreover, Dr. Yasko posted recently in FB a new study linking methylation and diabetes Mellitus type II. I could go on and on...

2. NO/ONOO- disregulation cycle, by Martin, L. Pall. For me it is a consequence of the above, but it could be argued the opposite. Ether way, It does exist in CFS, it very wisely explains most of our symptoms, and according to the author, it's the bases of CFS/ ME/ FM/ GWS and MQS, and it could explain many other conditions as well.

3.If the above 2 theories approaches these diseases from a bioquemical perspective, Professor Kenny De Meirleir's new theory based on Human Endoretroviruses (HERVs) focuses on the microbiological picture, and it explains how HERVs, he and his team found in the resident macrophages of the gut (plasmatic dendritic cells), are expressing proteins that act as superantigens. These proteins, throughout 2 mechanisms cause autoimmunity, excessive non specific T cell proliferation, B cell disregulation, and systemic inflammation . The last two could explain CFS symptoms, and moreover, these mechanisms would explain many autoimmune disorders (studies in this line are being carried out for MS or E. S. Lupus for instance.

The 3 theories fit together very nicely, and are capable of explaining how toxins, viral (EBV, HHV-6), bacterial (Lyme, Bartonela) or fungal infections would play a pivotal role in perpetuating the disease.

From an immunological point of view, however, something very interesting occurs. For instance in MS there's a dominance of Th1 response, while on CFS there a dominance of Th2 immunity. On the other hand, Lyme diseases lowers the CD57 while leaving a characteristic inflammatory trace, that can be seen by pro-inflmatory cytokines.

We still need to wait for the videos of the conference. If the CFS organization in charge of this (ASSSEM) has not planned it, I will translate the gist of the videos myself. There's a lot of technical information there that was shown.

It seems that there're 2 main objectives: 1. To study the role of the T regulatory lymphocytes in order to better understand the CFS pathophysiology and hopefully to be able to develop target drugs and 2. Try to validate two potential biomarkers they have found, I hope unique to CFS. Well, if this was true, then this would mean a turning point for all PWCFS, beyond any doubt. But let's be cautious here and wait.

But the MAIN achievement I think this study could bring I think is the attention of the media, the pharmaindustry and the scientific field, given the fact that they are well known, respected and top researchers in HIV, and now they have committed to CFS... This gives credit to whatever they find, even if it is new or just confirmatory data, and even if they don't find a unique biomarker. Think that we already have unique biomarkers, such as the mitochondrial profile (with a P<=0.001). But no one pays attention to it. On the contrary, there're well accepted syndromes with no specific markers, but if patients fit a given criteria, including symptoms and some tests results, the diagnosis is perfectly valid.

In conclusion: There're 2 different trends in CFS research. One is looking for the cause, and the other, maybe more boring, is finding biomarkers. Both are necessary and may perfectly help and benefit from each other.

So yes, everything points to several diseases having a common bioquemical and/or immunologic footprints (probably including the same pathogens involved). Probably in what concerns to CFS, they will find different subsets of patients, with different patterns of similar alterations, that will correlate with certain kind of symptoms or distinct severity of these symptoms, as the authors of the Irsi Caixa study state, from the results found.

Best!
Sergio
 
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CD57 NK cells arise from the further differentiation of CD56bright cells.

Model of human CD56dim NK-cell differentiation. Different experimental evidence supports the notion that peripheral blood CD56bright give rise to CD56dim NK cells. These 2 subsets differ in proliferative potential, cytolytic activity, and capability of secreting IFN-γ or TNF-α upon cytokine stimulation. With respect to cytokine secretion, however, recent studies revealed that CD56dim are capable of rapid secretion upon cell triggering via activating receptors (Fauriat et al12 and A. De Maria et al, personal communication). Two independent articles showed that CD56dim cells can be further fractionated into different cell subsets on the basis of their surface markers and function. As depicted in this schematic figure, the progression of CD56dim toward putative terminally differentiated NK cells is accompanied by the progressive loss of their proliferative capacity and the acquisition of more efficient cytolytic activity. Different maturational stages can be identified on the basis of the progressive down-regulation of CD94 and the expression of (1or more) KIRs and of CD16. CD57 expression is acquired at later stages and marks terminally differentiated cells with high cytolytic activity but very low proliferative potential.
From: http://bloodjournal.hematologylibrary.org/content/116/19/3689.full

What is interesting is that Brenu et al has noted in several studies, decreased cytotoxic activity of CD56bright cells.

It seems the cytotoxic activity of the innate immune system is being suppressed along with a strong anti-inflammatory response of the active immune system, particularly with high levels of glucocorticoid receptors (which themselves can promote the expression of anti-inflammatory cytokines in the absence of glucocorticoids).

It it is not as simple as TH2 vs TH1...