Altered TRPM7-Dependent Calcium Influx in Natural Killer Cells of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Patients

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a disabling multisystemic condition. The pathomechanism of ME/CFS remains unestablished; however, impaired natural killer (NK) cell cytotoxicity consistent feature this Calcium (Ca2+) crucial for NK effector functions. Growing research recognises Ca2+ signalling dysregulation in patients and implicates transient receptor potential ion channel dysfunction. TRPM7 (melastatin) was recently considered the pathoaetiology as it participates several Ca2+-dependent processes that are central to which may be compromised ME/CFS. TRPM7-dependent influx assessed cells isolated from n = 9 age- sex-matched healthy controls (HCs) using live fluorescent imaging techniques. Slope (p < 0.05) significantly reduced compared with HCs following activation. Half-time maximal response amplitude 0.001) were desensitisation. Findings investigation suggest agonism increased antagonism relative HCs. outcomes reported here potentially reflect TRPM3 dysfunction identified condition suggesting TRP channelopathy.