Open Medicine Foundation (OMF) is proud to share details of a new OMF-funded publication from Christopher Armstrong, Ph.D., and colleagues: “In vitro B cell experiments explore the role of CD24, CD38 and energy metabolism in ME/CFS.” Read now!
From the Desk of Dr. Armstrong, Director of the OMF Supported
Melbourne ME/CFS Collaboration:
In this paper, we explored how the behavior of B cells (a type of immune cell in the blood) differs between individuals with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and healthy controls. Previous research had shown that B cells from ME/CFS patients had higher levels of a protein on the cell surface called CD24. We wanted to understand the connection between CD24, B cell energy metabolism, and mitochondrial mass.
We conducted experiments using purified B cells from both ME/CFS patients and healthy controls, stimulating the cells in a lab setting to observe changes. Each set of experiments on one patient’s cells took a week. It was quite intensive. This is why the population number is small, and we would call this a “preliminary” or “pilot study.”
Even with a small sample size, the detailed characterization of the B cells was able to identify a few interesting details.
- B cells from ME/CFS patients exhibited lower mitochondrial mass.
- ME/CFS B cells took longer to lose CD24 protein from the surface when stimulated compared to those from healthy controls.
- CD38 protein was found to be significantly increased in frequency and expression on ME/CFS B cells, CD38 protein is well known in the aging world as it dictates the reduction of NAD+, a critical molecule for mitochondrial energy production.
- Metabolomic analysis showed that ME/CFS B cells consumed more essential amino acids during proliferation, suggesting an increased need for these substrates to support cell growth and survival. This aligns with previous findings of reduced amino acids in biological fluids from ME/CFS patients.
Overall, this study provides a detailed characterization of B cell behavior in ME/CFS, highlighting abnormalities in CD24 and CD38 expression, mitochondrial mass, and metabolic pathways. The findings suggest disruptions in normal energy production pathways in ME/CFS patients, emphasizing the need for further research with larger sample sizes to validate these results and explore potential therapeutic implications.
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