new Maes article about autoimmunity in ME

[msf]

http://www.ncbi.nlm.nih.gov/pubmed/25617880http://www.ncbi.nlm.nih.gov/pubmed/25617880

I thought the suggested mechanism for the increase in autoimmunity was particularly interesting.

 

[msf]

Oops, the mechanism was suggested here: http://www.ncbi.nlm.nih.gov/pubmed/22614823

 

[OverTheHills]

http://www.ncbi.nlm.nih.gov/pubmed/25617880http://www.ncbi.nlm.nih.gov/pubmed/25617880

.

this link doesn't work for me
OTH

 

[msf]

Sorry, just go to Pubmed and search for w maes, it's the first article.

 

[msf]

The first article basically claims that anti-oxidants reduce the auto-immune epitopes described in the second one.

 

[msf]

reduce the number, that is.

 

[ahmo]

This is really interesting to me. I've been coming to understand and track the role of peroxynitrite, oxidative stress. And I've been having good results using antioxidants, especially reseveratrol.

From the abstract linked above:

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and depression are considered to be neuro-immune disorders (Maes and Twisk, BMC Medicine 8:35, 2010). There is also evidence that depression and ME/CFS are accompanied by oxidative and nitrosative stress (O&NS) and by increased autoantibodies to a number of self-epitopes some of which have become immunogenic due to damage by O&NS.

Here's a full length, 2014 paper. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3964747/
Oxidative and Nitrosative Stress and Immune-Inflammatory Pathways in Patients with Myalgic Encephalomyelitis (ME)/Chronic Fatigue Syndrome (CFS)

And an interesting related piece about the same mechanism in depression:
http://www.artdevanyonline.com/1/post/2012/12/depression-first-heal-the-brain.html

 

[msf]

Other interesting aspects of oxidative stress are its effects on the mitochondria and also it's role in endothelial dysfunction, both of which are suspected in ME patients.

 

[Woolie]

I can't seem to access the full article, but looks from the abstract like an open-label study. Would be nice to see if its still works in a double-blind, placebo-controlled trial.

 

[msf]

Yeah, but I think the interesting thing was that a reduction in auto-immune epitopes (apparently) correlated with improvement in symptoms. If true, this suggests that these epitopes are an important element in ME.

 

[Woolie]

Yeah, but I think the interesting thing was that a reduction in auto-immune epitopes (apparently) correlated with improvement in symptoms. If true, this suggests that these epitopes are an important element in ME

True, @msf, this is unlikely to be a placebo effect.

 

[alex3619]

Is this the second thread on this?

 

[leokitten]

@Jonathan Edwards if you have time I would love to know what you think about the two papers mentioned in this thread, in particular this idea:

Prolonged elevation of O&NS species damages lipids, proteins, DNA and other structures to such an extent that they lose immunogenic tolerance and autoantibodies are formed against them. Details of immune responses generated against these O&NS modified neoepitopes can be found in Morris and Maes.

And this:

Increased IgM-related autoimmune responses to oxidative specific epitopes (OSEs), including malondialdehyde (MDA), oleic acid and phosphatidyl inositol (Pi), and nitroso-(NO)-adducts, including NO-tryptophan (NOW), NO-arginine and NO-cysteinyl, are frequently observed in ME/CFS.

 

[Jonathan Edwards]

@Jonathan Edwards if you have time I would love to know what you think about the two papers mentioned in this thread, in particular this idea:

And this:

I think we have discussed these papers before. I don't think I could make much of them last time. I worry that the authors do not really have a grasp of the concept of immunological tolerance - which may be why they talk of molecules losing 'immunogenic tolerance', which is not a phrase any immunologist I know would use. (Tolerance is a property of an immune system, not an antigen.) It would be interesting if ME/CFS IgM was found to bind to oxidised molecules more than well matched healthy controls, but if that was found it would be better simply to report that with some substantive data numbers in the abstract rather than waffle on about autoimmunity. (Binding of immunoglobulin to degraded organic molecules is probably quite a normal phenomenon.)