期刊
JOURNAL OF IMMUNOLOGY
卷 200, 期 8, 页码 2529-2534出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1701467
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- Deutsche Forschungsgemeinschaft [Sonderforschungsbereich (SFB) 688, TP-A18, TP-A10, TP-A22, TRR152]
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.
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