Magawa, Chandi Tabeth, Eaton-Fitch, Natalie, Muraki, Katsuhiko et al. · BMC immunology · 2026 · DOI
Researchers compared immune cells called natural killer cells from people with ME/CFS and healthy controls, focusing on how calcium moves in and out of these cells. They observed that calcium entry into cells was reduced in ME/CFS, but calcium accumulation in the energy-producing part of the cell (mitochondria) was higher. This is a preliminary finding from a small study that may help explain some immune dysfunction in ME/CFS, but much more research is needed before drawing conclusions about what this means for patients.
ME/CFS is characterised by reduced natural killer cell function, and understanding the ion channels that regulate calcium signalling in these cells may help explain immune dysregulation in the disease. This study identifies a specific cellular pathway (TRPM3-mediated calcium entry) that appears altered in ME/CFS, which could be a target for future mechanistic or therapeutic research. However, it remains unknown whether these calcium changes directly contribute to symptom burden or post-exertional malaise.
This study does not establish that TRPM3 dysfunction causes ME/CFS or that correcting it will treat the disease. The small sample size (N=10 per group) and single-occasion measurements do not confirm the clinical significance of these calcium changes or their relationship to PEM, fatigue severity, or symptom progression. It does not identify a root cause of ME/CFS, only one candidate cellular abnormality associated with the disease.
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 →
The first block is for the primary paper and is the citation you should use in research work. The atlas-snapshot line only applies if you are specifically referring to this atlas’s reading of the paper on the date shown.
Primary citation
Magawa, Chandi Tabeth, Eaton-Fitch, Natalie, Muraki, Katsuhiko, & Marshall-Gradisnik, Sonya (2026). Deficient TRPM3-linked mitochondrial Ca<sup>2+</sup> influx in natural killer cells associated with myalgic encephalomyelitis/chronic fatigue syndrome.. BMC immunology. https://doi.org/10.1186/s12865-026-00849-1
BibTeX
@article{mecfsatlas-magawa-2026-deficient-trpm3,
author = {Magawa, Chandi Tabeth and Eaton-Fitch, Natalie and Muraki, Katsuhiko and Marshall-Gradisnik, Sonya},
title = {Deficient TRPM3-linked mitochondrial Ca<sup>2+</sup> influx in natural killer cells associated with myalgic encephalomyelitis/chronic fatigue syndrome.},
journal = {BMC immunology},
year = {2026},
doi = {10.1186/s12865-026-00849-1},
note = {PubMed: 42177403},
url = {https://www.mecfsatlas.com/evidence/magawa-2026-deficient-trpm3},
}Atlas snapshot reference
ME/CFS Atlas. Generator v1 / Scanner v1.4 / policy v0.1. Accessed 2026-05-25. https://www.mecfsatlas.com/evidence/magawa-2026-deficient-trpm3
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