Multi-omics identifies lipid accumulation in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome cell lines: a case-control study, 2026, Missailidis et

[jnmaciuch]

Yes I know that

My bad, I thought you were asking “and why” there were missing values

 

[Evergreen]

I wouldn't relate these observations to body-wide issues or dietary aspects. This observation is most likely to be a consequence of a cell type specific effect, and even if it wasn't, we haven't got evidence of that yet.

Thank you for confirming that I can safely forget about this!

Really hope you start feeling better soon.

 

[Tree]

Thank your doing this research, the ME field seems to be very challenging being underfunded and with little support.

Thank you aswell for explaining everything for even lay people.

Hope you feel better soon and hope to see more of your research.

 

[jnmaciuch]

Here’s the paper I was thinking of from Bali Pulendran’s lab about lipid regulation in B cells:

SREBP signaling is essential for effective B cell responses - PMC

Our previous study using systems vaccinology identified an association between the sterol regulatory binding protein (SREBP) pathway and humoral immune response to vaccination in humans. To investigate the role of SREBP signaling in modulating ...

pmc.ncbi.nlm.nih.gov

It identified the transcription factor SREBP as the “master regulator” of B cell lipid metabolism—though other transcription factors could (and almost certainly do) also influence SREBP or subsets of its target genes [edit: and that is probably cell-type specific]

 

[Violeta]

I think the most obvious and potentially relevant consequence would be differences in cell membrane fluidity and lipid raft dynamics (due to the specific classes of compounds involved, including cholesterol). This would affect BCR engagement.

This study is about underproduction of phosphatidylserine and BCR/CD22 and lymphoma.

Phosphatidylserine synthesis controls oncogenic B cell receptor signaling in B cell lymphoma​

Phosphatidylserine synthesis controls oncogenic B cell receptor signaling in B cell lymphoma - PMC

Omi et al. identify phosphatidylserine (PS) synthesis as a key metabolic vulnerability in B cell receptor (BCR)-positive B cell lymphomas. Inhibition of PS synthesis causes an imbalanced phospholipid metabolism via membrane contact-based lipid ...

pmc.ncbi.nlm.nih.gov

I can't find a study about overproduction of phosphatidylserine and BCR/CD22, but I'll keep looking.

The principal role of CD22 is to regulate the BCR. CD22 is a membrane receptor found on B cells and is a member of the Siglec family of proteins ...

​

 

[Violeta]

It does seem strange that the B cells of pwME/CFS had higher levels of phosphatidylserine than control group, but at the same time we have seen phosphatidylserine recommended for people with ME/CFS, and have seen people say they benefitted from it. Is that a clue?

 

[Jonathan Edwards]

at the same time we have seen phosphatidylserine recommended for people with ME/CFS, and have seen people say they benefitted from it. Is that a clue?

I rather doubt it. I suspect that it is recommended simply because it sounds like a 'supplement' to alternative practitioners. And some people will always say they benefited from whatever.

 

[Violeta]

From Linus Pauling website:

The long-chain omega-3 polyunsaturated fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), and the B-vitamin niacin (nicotinic acid) have potent triglyceride-lowering effects.

There is niacin in my B complex, but I have difficulty taking it separately.

@mariovitali, interesting that the pro-resolving mediators is based on EPA and DHA. I don't know if that's just a coincidence.
Maybe it is that triglycerides interfere with autophagy.

 

[DMissa]

We don't know if the observations seen here in a relatively small cohort of immortalised cell lines reflect a biological reality in the patient, and if they did what the relationship (if any) is with a disease process. So I would not endorse any particular intervention based on this study.

What I want to get funding to do next (with relation to this study) is related measurements on primary immune populations while coupled with relevant measurements of function that could plausibly be related to symptoms. But that's still just an idea in the oven and I am also weighing up its value against other avenues we are uncovering in other projects.

In case this was not apparent I am the first author on the paper

 

[hotblack]

What I want to get funding to do next (with relation to this study) is related measurements on primary immune populations while coupled with relevant measurements of function that could plausibly be related to symptoms

Can you detail a bit more about what this would look like? A wider breakdown of B and T cell populations? Would it include information about innate immune cells too? When you say function do you mean function of the cells? What sort of measures would this include?

I’m just trying to understand what sort of information we could get from such a study.

 

[V.R.T.]

other avenues we are uncovering in other projects.

Exciting that you are uncovering other avenues! Are any of those projects written up/submitted or are they still ongoing?