Journal
INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH
Volume 18, Issue 22, Pages -Publisher
MDPI
DOI: 10.3390/ijerph182211879
Keywords
myalgic encephalomyelitis; chronic fatigue syndrome; natural killer cell; transient receptor potential melastatin 7; IL-2; PIP2
Funding
- Stafford Fox Medical Research Foundation [489798]
- McCusker Charitable Foundation [49979]
- Buxton Foundation [4676]
- Blake Beckett Trust Foundation [4579]
- Alison Hunter Memorial Foundation [4570]
- Change for ME Charity [4575]
- Henty Community [4879]
- Henty Lions Club [4880]
- Mason Foundation [47107]
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ME/CFS is a complex disorder associated with significant disability, and impaired NK cell cytotoxicity is a consistent feature. Research suggests that dysregulated calcium signaling and dysfunction of channels like TRPM3 are implicated in the pathophysiology of the disease.
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex multisystemic disorder responsible for significant disability. Although a unifying etiology for ME/CFS is uncertain, impaired natural killer (NK) cell cytotoxicity represents a consistent and measurable feature of this disorder. Research utilizing patient-derived NK cells has implicated dysregulated calcium (Ca2+) signaling, dysfunction of the phosphatidylinositol-4,5-bisphosphate (PIP2)-dependent cation channel, transient receptor potential melastatin (TRPM) 3, as well as altered surface expression patterns of TRPM3 and TRPM2 in the pathophysiology of ME/CFS. TRPM7 is a related channel that is modulated by PIP2 and participates in Ca2+ signaling. Though TRPM7 is expressed on NK cells, the role of TRPM7 with IL-2 and intracellular signaling mechanisms in the NK cells of ME/CFS patients is unknown. This study examined the effect of IL-2 stimulation and TRPM7 pharmacomodulation on NK cell cytotoxicity using flow cytometric assays as well as co-localization of TRPM7 with PIP2 and cortical actin using confocal microscopy in 17 ME/CFS patients and 17 age- and sex-matched healthy controls. The outcomes of this investigation are preliminary and indicate that crosstalk between IL-2 and TRMP7 exists. A larger sample size to confirm these findings and characterization of TRPM7 in ME/CFS using other experimental modalities are warranted.
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