study examines link between immune dysfunction and metabolis in me

[Hufsamor]

https://meaustralia.net/2018/11/14/...kk_1Um8dqn9UdSmavYHxMH7ohieIKF11A2NHH2LqadIiA

 

[Hufsamor]

https://www.frontiersin.org/articles/10.3389/fimmu.2018.02421/full

We conclude that CD24 expression on B cells is related to energy metabolism throughout differentiation and that its role differs between B cell subsets.

 

[Moof]

Thanks for posting this – it's a bit easier to understand than the original article.

 

[ljimbo423]

Thanks for posting this @Hufsamor!

“More and more papers are showing that altered cell metabolism alters the function of the cell and the altered metabolism of immune cells would be no exception” said Dr Armstrong.

“The CD24 marker may make cells more prone to react to anything, for example if there’s a signal, they’ll make sure it is stronger.

It may make cells more sensitive, whether good or bad.

The increased CD24 could be the reason for increased immune activation in ME/CFS patients, as the CD24 may increase the chance for activation,” said Dr Armstrong.

“Abnormalities in energy pathway usage has already been described as an important feature in understanding the pathophysiology and etiology in ME/CFS.

The metabolic anomalies described in sera from patients with ME/CFS have been proposed to be regulated by increased AMPK phosphorylation.

This would thus appear to be confirmed by the finding of increased expression of CD24 on B cells from ME/CFS patients and its relationship to AMPK and surrogate measures of glycolysis, namely glucose consumption and lactate production as observed in this study.”

EDIT- "phosphorylated" AMPK is "activated" AMPK.

 

[ScottTriGuy]

I thought this was interesting since some ME folks improved on Metformin: https://www.ncbi.nlm.nih.gov/pubmed/29343420

"...the effect of the antidiabetic drug metformin on lipogenesis inhibition and fatty acid oxidation stimulation was enhanced by combination treatment with small-molecule AMPK activators in primary hepatocytes from mice and humans. Overall, these results demonstrate that AMPK downregulation is not a triggering factor in fatty liver development but in contrast, establish the therapeutic impact of pharmacological AMPK re-activation in the treatment of fatty liver disease."

@mariovitali