Balinas, Cassandra, Cabanas, Helene, Staines, Donald et al. · Journal of translational medicine · 2019 · DOI
This study looked at immune cells called NK cells in people with ME/CFS, focusing on special channels on their surface called TRPM2 that control calcium flow. Researchers found that ME/CFS patients had higher levels of these TRPM2 channels compared to healthy people, and their NK cells were less effective at fighting infections. When researchers tried two different drugs to modify these channels, the drugs reduced TRPM2 levels but did not improve the cells' ability to fight infections.
NK cell dysfunction is a hallmark of ME/CFS, and understanding the specific cellular mechanisms—like calcium regulation through TRPM2 channels—may reveal why immune responses are impaired. This research provides potential targets for future therapies aimed at restoring NK cell function and could eventually lead to treatments that improve immune competence in ME/CFS patients.
This study does not prove that TRPM2 overexpression causes ME/CFS or that correcting TRPM2 levels will cure the disease. It does not establish whether the TRPM2 changes are a cause or consequence of immune dysfunction, and the lack of cytotoxicity improvement with drug treatment suggests TRPM2 targeting alone may be insufficient. The small sample size and in vitro design limit generalizability to real-world disease mechanisms.
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 →
Contribute
Private, reviewed by a human. Not a public comment thread.