Emerging Role of Autoimmunity in ME/CFS

[MeSci]

Just the abstract so far:

Mol Neurobiol. 2013 Sep 26. [Epub ahead of print]
The Emerging Role of Autoimmunity in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/cfs).

Morris G, Berk M, Galecki P, Maes M.

Source

Mumbles Head, Pembrey, Llanelli, UK.

Abstract

The World Health Organization classifies myalgic encephalomyelitis/chronic fatigue syndrome (ME/cfs) as a nervous system disease. Together with other diseases under the G93 heading, ME/cfs shares a triad of abnormalities involving elevated oxidative and nitrosative stress (O&NS), activation of immuno-inflammatory pathways, and mitochondrial dysfunctions with depleted levels of adenosine triphosphate (ATP) synthesis. There is also abundant evidence that many patients with ME/cfs (up to around 60 %) may suffer from autoimmune responses. A wide range of reported abnormalities in ME/cfs are highly pertinent to the generation of autoimmunity. Here we review the potential sources of autoimmunity which are observed in people with ME/cfs. The increased levels of pro-inflammatory cytokines, e.g., interleukin-1 and tumor necrosis factor-α, and increased levels of nuclear factor-κB predispose to an autoimmune environment. Many cytokine abnormalities conspire to produce a predominance of effector B cells and autoreactive T cells. The common observation of reduced natural killer cell function in ME/cfs is a source of disrupted homeostasis and prolonged effector T cell survival. B cells may be pathogenic by playing a role in autoimmunity independent of their ability to produce antibodies. The chronic or recurrent viral infections seen in many patients with ME/cfs can induce autoimmunity by mechanisms involving molecular mimicry and bystander activation. Increased bacterial translocation, as observed in ME/cfs, is known to induce chronic inflammation and autoimmunity. Low ATP production and mitochondrial dysfunction is a source of autoimmunity by inhibiting apoptosis and stimulating necrotic cell death. Self-epitopes may be damaged by exposure to prolonged O&NS, altering their immunogenic profile and become a target for the host's immune system. Nitric oxide may induce many faces of autoimmunity stemming from elevated mitochondrial membrane hyperpolarization and blockade of the methionine cycle with subsequent hypomethylation of DNA. Here we also outline options for treatment involving rituximab and endotherapia.

PMID: 24068616 [PubMed - as supplied by publisher]

 

[Marlène]

Tnx, I will send this to my rheumatologist.

 

[A.B.]

I'm VERY interested in the full article, but don't want to pay for it. Has anyone been able to find a copy somewhere on the internet?

 

[Bob]

I'm VERY interested in the full article, but don't want to pay for it. Has anyone been able to find a copy somewhere on the internet?

You can read the first two pages for free here, if you click on 'look inside' at top-right of webpage:
http://link.springer.com/article/10.1007/s12035-013-8553-0#page-1

 

[nandixon]

The full text of the article is available here as a downloadable pdf file:
http://www.researchgate.net/publica..._Syndrome_(MEcfs)/file/9c960524b4ed6dfb0b.pdf

 

[aimossy]

This is soooooo worth reading and taking in, I have only read parts and can't take it in properly.I wonder what professor Edwards makes of it. Or anyone who has the good science brain!
There is lots to take in.

 

[Jonathan Edwards]

I had a look at the paper. The introductory sections give quite a good review of some of the evidence for autoimmunity being relevant to ME. Later sections of the paper, however, seem to focus on fashionable ideas that have largely proved unhelpful, or at least never really made sense and never been supported by any evidence, to my way of thinking - molecular mimicry, T cell autoreactivity and a non-antibody mediated role for B cells. They actually quote our use of rituximab as support for the idea that there is a non-antibody mediated role for B cells but the data from use of rituximab are clearly against this conclusion. The delayed response indicates an effect on autoantibody levels, not help to T cells. Sadly this seems to be a rewrite of the received wisdom that gets perpetuated in the review journals. Still, at least I am all in favour of airing of ideas about autoimmunity in ME.