Study Examines Link between Immune Dysfunction and Metabolism in ME

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This article was first published on ME Australia
An international collaboration of scientists, including Fane Mensah, Jo Cambridge and Australia’s Chris Armstrong, investigated the relationship between CD24 expression and B cell maturation and found CD24 expression on B cells is related to energy metabolism and that its role differs between B cell subsets.
The study – CD24 Expression and B Cell Maturation Shows a Novel Link with Energy Metabolism: Potential Implications for Patients With Myalgic Encephalomyelitis/Chronic Fatigue Syndrome – by Mensah et al was published in Frontiers of Immunology in October 2018. Mensah works at the Centre of Rheumatology Research at University College London and collaborates internationally. He visited Australia earlier this year and was profiled in ‘Meet the Scientists: Fane Mensah’.
The study is trying to reveal a potential link between previous observations of altered metabolism and immune dysfunction in people with ME. The study examined nine people with ME/CFS (Canadian Consensus Criteria) and eight healthy controls with a median age of 33.
The paper says there was a significant correlation between CD24 expression on B cells and the usage of glucose and secretion of lactate in vitro.
“The dynamic nature of B cells is a good model to observe changes in energy demand, in which CD24 seems to play an important role,” said Fane Mensah.
“There was more CD24 expression on B cells in ME patients. More CD24 was associated with more glucose and less lactate, which may mean that more CD24 is associated with less glycolysis,” explained Chris Armstrong.
“AMPK phosphorylation reduces glycolysis and we observed that AMPK was more phosphorylated in maturing B cells that maintained CD24 markers.  AMPK phosphorylation might explain the metabolism changes observed in ME/CFS patients and may also be implicated in increasing the CD24 expression on B cells that we have observed.”
“CD24 is a cell adhesion molecule known to mediate signal transduction, it currently isn’t well described but it has a variety of roles that may indicate that it may function to potentiate signals (increase sensitivity).”
This study of dysregulation in CD24 expressing B cells confirms the findings of other studies done using different methods.
“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 Armstrong.
“The study is important because it potentially forms a connection between the immune system and metabolism. The CD24 marker increase shows a strong relationship to energy metabolism.”

“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 Armstrong.

“As little is known about CD24 at this stage, it is pertinent to follow up with more research into its function.”
“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.”
“We hope to be doing more work on this,” said Armstrong.
“Interdisciplinary studies between immunology and metabolism are of great interest in ME/CFS, I hope more will follow,” said Mensah.
Read the full paper .
 

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