Editors' ChoiceImmunology

Magnesium to the Rescue

Science Signaling  16 Jul 2013:
Vol. 6, Issue 284, pp. ec165
DOI: 10.1126/scisignal.2004508

Individuals with XMEN [X-linked immunodeficiency with Mg2+ defect, Epstein-Barr virus (EBV) infection, and neoplasia] disease are genetically deficient for expression of MAGT1, a magnesium transporter. Chaigne-Delalande et al. sought to better understand why these individuals are chronically infected with EBV at high viral loads and are susceptible to the development of lymphomas. CD8+ T cells and natural killer cells, which help to keep EBV infection in check, exhibited reduced cytotoxicity owing to their lower expression of the cell surface receptor NKG2D, which triggers cytolysis upon ligation. Magnesium supplementation in vitro and also in two XMEN patients restored levels of free Mg2+, increased NKG2D expression, and resulted in reduced amounts of EBV+ cells, suggesting that this may be an effective therapeutic approach for XMEN patients.

B. Chaigne-Delalande, F.-Y. Li, G. M. O’Connor, M. J. Lukacs, P. Jiang, L. Zheng, A. Shatzer, M. Biancalana, S. Pittaluga, H. F. Matthews, T. J. Jancel, J. J. Bleesing, R. A. Marsh, T. W. Kuijpers, K. E. Nichols, C. L. Lucas, S. Nagpal, H. Mehmet, H. C. Su, J. I. Cohen, G. Uzel, M. J. Lenardo, Mg2+ regulates cytotoxic functions of NK and CD8 T cells in chronic EBV infection through NKG2D. Science 341, 186–191 (2013). [Abstract] [Full Text]