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Characterising B cells in ME/CFS

STUDY AIM
This study aims to broadly evaluate B cell subsets, metabolism, viability, receptors, and antibodies in people with ME/CFS.
INVESTIGATORS
  • Christopher Armstrong, PhD
  • Paul Gooley, PhD
  • Jo Cambridge, PhD
RESULTS

This study is complete. The paper is here.

STUDY HYPOTHESIS AND DESCRIPTION

A number of anomalies in B cells have been observed in the few studies conducted on ME/CFS patients. We want to expand this area of research to better understand these changes and determine if there are any potential anomalies in antibody production or metabolism that could be driving altered immune response.

 

OUTCOME SUMMARY

In this paper, we explored how the behaviour 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 characterisation 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 characterisation of B cell behaviour 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, emphasising the need for further research with larger sample sizes to validate these results and explore potential therapeutic implications.
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