Visser, J, Blauw, B, Hinloopen, B et al. · The Journal of infectious diseases · 1998 · DOI
This study looked at immune cells called CD4 T cells from ME/CFS patients and found they produced less of a protective immune protein called interferon-gamma compared to healthy people. Interestingly, these cells were also much more sensitive to dexamethasone, a steroid medication—it took 10-20 times less of the drug to suppress certain immune functions in ME/CFS patients than in controls. This suggests that the stress hormone system and immune system may be working abnormally together in ME/CFS.
This research provides evidence that ME/CFS involves both a dysregulated stress hormone system and abnormal immune responses at the cellular level. Understanding why ME/CFS immune cells are hypersensitive to glucocorticoids could help explain the characteristic post-exertional malaise and guide development of targeted immune therapies. These findings support the biological basis of ME/CFS rather than viewing it as purely psychological.
This study does not prove that altered glucocorticoid sensitivity causes ME/CFS symptoms or that it is the primary driver of disease. It cannot establish causation or explain why this abnormality develops. The findings are from cultured cells in a laboratory and may not fully reflect the complexity of immune dysfunction in living patients with ME/CFS.
About the PEM badge: “PEM required” means post-exertional malaise was an explicit required diagnostic criterion for participant inclusion in this study — not that PEM was studied, observed, or discussed. Studies using criteria that do not require PEM (e.g. Fukuda, Oxford) are tagged “PEM not required”. How the atlas works →
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