| First Author | Gotru SK | Year | 2018 |
| Journal | J Immunol | Volume | 200 |
| Issue | 8 | Pages | 2529-2534 |
| PubMed ID | 29581357 | Mgi Jnum | J:260923 |
| Mgi Id | MGI:6152069 | Doi | 10.4049/jimmunol.1701467 |
| Citation | Gotru SK, et al. (2018) Cutting Edge: Imbalanced Cation Homeostasis in MAGT1-Deficient B Cells Dysregulates B Cell Development and Signaling in Mice. J Immunol 200(8):2529-2534 |
| abstractText | 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 Mg(2+) homeostasis in T lymphocytes. Using Magt1-knockout mice (Magt1(-/y) ), we show that Mg(2+) homeostasis was impaired in Magt1(-/y) B cells and Ca(2+) 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. |
