Cation homeostasis, in relation to various immune-suppressive diseases, is a 
novel field of investigation. Recently, patients with a loss-of-function 
mutation in magnesium transporter 1 (MAGT1) were reported to present a 
dysregulated Mg2+ homeostasis in T lymphocytes. Using Magt1-knockout mice 
(Magt1-/y ), we show that Mg2+ homeostasis was impaired in Magt1-/y B cells and 
Ca2+ influx was increased after BCR stimulation, whereas T and NK cell function 
was unaffected. Consequently, mutant B cells displayed an increased 
phosphorylation of BCR-related proteins differentially affecting protein kinase 
C activation. These in vitro findings translated into increased frequencies of 
CD19+ B cells and marginal zone B cells and decreased frequencies of plasma 
cells among CD45+ splenocytes in vivo. Altogether, our study demonstrates for 
the first time, to our knowledge, that abolished MAGT1 function causes 
imbalanced cation homeostasis and developmental responses in B cells. Therefore, 
this study might contribute to a further understanding of B cell-related 
pathologies.