Journal
SCIENCE
Volume 341, Issue 6142, Pages 186-191Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1240094
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Funding
- Division of Intramural Research, National Institute of Allergy and Infectious Diseases
- National Cancer Institute, NIH
- Medical Scientist Training Program at the University of California-San Francisco
- NIH
- Pharmacology Research Associate Training (PRAT) program
- National Institute of General Medical Sciences, NIH
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The magnesium transporter 1 (MAGT1) is a critical regulator of basal intracellular free magnesium (Mg2+) concentrations. Individuals with genetic deficiencies in MAGT1 have high levels of Epstein-Barr virus (EBV) and a predisposition to lymphoma. We show that decreased intracellular free Mg2+ causes defective expression of the natural killer activating receptor NKG2D in natural killer (NK) and CD8(+) T cells and impairs cytolytic responses against EBV. Notably, magnesium supplementation in MAGT1-deficient patients restores intracellular free Mg2+ and NKG2D while concurrently reducing EBV-infected cells in vivo, demonstrating a link between NKG2D cytolytic activity and EBV antiviral immunity in humans. Moreover, these findings reveal a specific molecular function of free basal intracellular Mg2+ in eukaryotic cells.
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