Is the key pathology of ME/CFS in bone marrow?

[ryanc97]

Daratumumab targets bone marrow LLPCs. There's your answer....

 

[leokitten]

IRF5 Controls Plasma Cell Generation and Antibody Production via Distinct Mechanisms Depending on the Antigenic Trigger - PMC

Elevated levels of serum autoantibodies are a hallmark of systemic lupus erythematosus (SLE) and are produced by plasma cells in response to a variety of antigenic triggers. In SLE, the triggers are complex and may include both T ...

pmc.ncbi.nlm.nih.gov

 

[janice]

Could you collect bone marrow post mortum and still get a useful sample? Because ME/CFS patients die every week, many of which would donate their bodies to science if there is someone wanting to take the body and do more detailed studies on it. When it comes to invasive tests like this having registered sufferers willing to donate their body might well be the way to go, assuming what you need to look for is likely still viewable.

Couldn’t you take bone marrow sample from thigh like they do for leukaemia diagnosis / donation etc?
However my bone pain has been in a specific place for last 25+ years ie left shin bone plus left arm pit throb. After 20 yrs I found Aciclovir reduces these massively. Couldn’t a fine needle aspiration sample be taken at these sires. ?

 

[janice]

I think that is a useful point but bone marrow output of myeloid cells can respond pretty rapidly. I don't know details but after haemorrhage platelet numbers can go up within a few hours and I presume that is from marrow release. Similarly, with infection the neutrophil count can rise fivefold in a few hours.

I think the sort of mechanism proposed might be subject to overriding with acute signals much in the way that people talk of adrenaline overriding PEM in the very short term. Some also talk of getting better ME/CFS wise during infections. In RA we think there are underlying loops in immune memory but joint inflammation can appear and disappear over hours too.

I also think it is likely that any model like this might be one module of the process with neurological loops being other modules with some people's disease being almost entirely driven by immune loops and others' by brain loops but with both being involved to some degree in all.


If the immune loop is anything like the ones in RA and psoriasis (a B cell loop and a T cell loop) it seems they are consistent with just about any long term dynamic pattern in different cases. I think that may be an argument for invoking an adaptive clonal element but I am not sure. Just basing things on the rules of myeloid cells I would expect monozygotic twin concordance to be almost complete because they would meet relevant infections at some point and the pathways and regulatory steps engaged ought to be much the same.

Since the bone pain and arm pit throb which I have had for years began after glandular fever , this suggested to me clone of immune cells in bone and lymphoid tissue of left arm pit perhaps?