by Sasha Nimmo
Australian scientists at the National Centre for Neuroimmunlogy and Emerging Diseases at Griffith University published a new paper on reduced intracellular calcium mobilisation in Natural Killer (NK) immune cells and Transient Receptor Potential Melastatin 3 (TRPM3) cation channels. Authors say it ‘could suggest potential therapeutic targets and/or prognostic markers’.
“NK cells are an essential innate immune cell, responsible for recognising and inducing apoptosis of tumour and virus infected cells. Calcium is an essential component in mediating this cellular function. Transient Receptor Potential Melastatin 3 (TRPM3) cation channels have an important regulatory role in mediating calcium influx to help maintain cellular homeostasis.”
The paper said it particularly affects the brain, eye, cardiovascular system, gastrointestinal system and pancreas.
Lead author Dr Helene Cabanas is an emerging researcher who specialises in understanding calcium pathway signalling and their implications in physiological and pathophysiological processes. Her current research focus on the pathomechanism of Chronic Fatigue Syndrome / Myalgic Encephalomyelitis (CFS/ME), according to the NCNED website.
This study included six patients with Myalgic Encephalomyelitis (evaluated using the Fukuda, Canadian and International Consensus Criteria and all meeting the CCC), comprising four women and two men. Participants were excluded if they reported autoimmune diseases, cardiac disease, diabetes or other co-morbidities.
The study supports earlier findings from Griffith University and others, in finding reduced intracellular calcium mobilisation. This study used a different technique:
“The patch clamp technique is regarded as a gold standard for ion channel research and offers direct insight into ion channel properties through the characterization of ion channel activity. In this study, we characterised, for the first time, the TRPM3 ion channel current in isolated human NK cells.”
“While this study provides evidence of TRPM3 channel activity dysfunction in CFS/ME patients, this study is not without limitations with the low sample numbers. Indeed, these findings need to be validated in a larger cohort of patients.”
The study was supported by the Mason Foundation, McCusker Charitable Foundation, Stafford Fox Medical Research Foundation, Mr Douglas Stutt, Alison Hunter Memorial Foundation, Buxton Foundation, Blake Beckett Trust, Henty Donation and the Change for ME Charity.
Read more about what the calcium channel ion defects mean for patients and explanations from NCNED scientists in Calcium channel ion defects: research from Australia’s Griffith University.