ME/CFS Science Blog article - Immune findings in ME/CFS

[V.R.T.]

This was a really good and necessary article. I really hope it sunk in with some of the people who are pushing inflammation and viral persistance etc.

I did think there were a few notable omissions unless I missed them:

The finding of higher cd38 and cd24 in MECFS B cells.

Jackie Cliff's T cell findings.

The T cell dependant IFNy long covid finding from 2024 that Rosetta Stone may be trying to replicate.

 

[OrganicChilli]

I really hope it sunk in with some of the people who are pushing inflammation and viral persistance etc.

"We just haven't checked in all possible tissues yet. We just need the right combination of antivirals. We're looking for magic antibodies that haven't been discovered yet. We have different sub groups so our approach works, but we haven't identified the right patients."

My impression is that most people in the field care more about their ideology than producing results. Just like doctors they can't admit when they were wrong or don't know something.

 

[V.R.T.]

"We just haven't checked in all possible tissues yet.

Oh no is this us with immune signalling?

 

[EndME]

For Example:
In Graves’ disease (Morbus Basedow), antibodies activate the TSH receptor. Here, it is not the level alone that matters, but the functional effect at the receptor.

Seems like a bad example because the population level differences in TRabs between healthy people and people with Graves disease are massive and unlike anything seen in ME/CFS. The differences are so big that they are used for diagnosis even if the don't tell you everything about a single person and even if there may be deviations from the norm in any given individual. As has been mentioned countless of times before if you discount marginal differences in GPCR-aab because the argument is that population level differences don't matter, then you have no evidence for their role to begin with expect for of course negative evidence from B-cell trials.

 

[OrganicChilli]

Oh no is this us with immune signalling?

No, that's viral persistence.

 

[V.R.T.]

No, that's viral persistence.

Oh I know, I was joking because there's a lot of talk on here about immune signalling that might be happening in tissue and isnt detectable in blood!

I don't think it's the same at all I was just being silly.

 

[MeSci]

Great article - am still reading it, but in case no one else has spotted it, you have put 'TPSO' instead of 'TSPO' the last time in the section 'In the pipeline'.

I've found another tiny error - in the caption to the image in the paragraph 'Rituximab and daratumumab' it says "‘Clinical Immunology Principles and Practic', missing the final letter.

 

[Creekside]

With enough of that information in hand, the field of possibilities narrows appreciably.

The problem is that I get the impression we're doing the same studies over and over again.

Negative findings only narrow the field if they're actually accepted by the people who decide which studies get funding. That doesn't seem to be happening.

 

[Creekside]

Or worse, and this is what scares me, do we have the technological tools to understand MECFS?

We might (in retrospect someday) have the necessary tools, but we have to know where to look and what to look for, and to recognize it when it's in the data. We don't yet have the magic scanner that will scan the whole body and identify what's wrong.

As for deciding where to look, we're still discovering new body subsystems, even new organs, so how can we find a problem in some important body subsystem that is still undiscovered? The problem is even more difficult in the brain, with all its protections and sensitivity to damage. I expect that you can cut a sample of liver out and study it in detail (still functioning) in a petri dish, but studying brain cells isn't quite as easy.

I find more hope in the news stories about new discoveries in cellular functions, or new imaging/measuring technologies, than I do from newsletters from the OMF or other ME research organizations. Hmmm, I guess I must be convinced that we don't have the appropriate technology yet to discover ME's mechanism.

 

[Utsikt]

Negative findings only narrow the field if they're actually accepted by the people who decide which studies get funding. That doesn't seem to be happening.

It narrow the field for the researches that has a chance of making a difference, because they actually follows the evidence.

Lots of money will continue to be wasted on memes, but hopefully not all.

 

[MeSci]

Found another very small error in the paper:

Under 'General conclusion' it says "perhaps it’s another pieces of the puzzle".

Excellent piece, pulling everything together!

 

[Utsikt]

Treatments that increase NK-cell function, such as BioBran, Isoprinosine,and interferon-alpha, did not lead to an improvement in ME/CFS patients.

Is this evidence for the hypothesis that if there is reduced NK cytotoxicity, it is a side-effect of something else and not the cause of ME/CFS symptoms?

 

[Kitty]

Is this evidence for the hypothesis that if there is reduced NK cytotoxicity, it is a side-effect of something else and not the cause of ME/CFS symptoms?

Yeah, we don't seem to have much evidence of impaired cytotoxicity in the first place, do we. Given the length of time many of us have been ill, you'd probably expect a higher rate of malignancies and more severe responses to infections if it were an ongoing state. All we've seen is a suggestion of fewer viruses, which may or may not mean anything.