| First Author | Bhattacharyya S | Year | 2011 |
| Journal | J Exp Med | Volume | 208 |
| Issue | 4 | Pages | 823-39 |
| PubMed ID | 21464221 | Mgi Jnum | J:177319 |
| Mgi Id | MGI:5294733 | Doi | 10.1084/jem.20100945 |
| Citation | Bhattacharyya S, et al. (2011) NFATc1 affects mouse splenic B cell function by controlling the calcineurin--NFAT signaling network. J Exp Med 208(4):823-39 |
| abstractText | By studying mice in which the Nfatc1 gene was inactivated in bone marrow, spleen, or germinal center B cells, we show that NFATc1 supports the proliferation and suppresses the activation-induced cell death of splenic B cells upon B cell receptor (BCR) stimulation. BCR triggering leads to expression of NFATc1/alphaA, a short isoform of NFATc1, in splenic B cells. NFATc1 ablation impaired Ig class switch to IgG3 induced by T cell-independent type II antigens, as well as IgG3(+) plasmablast formation. Mice bearing NFATc1(-/-) B cells harbor twofold more interleukin 10-producing B cells. NFATc1(-/-) B cells suppress the synthesis of interferon-gamma by T cells in vitro, and these mice exhibit a mild clinical course of experimental autoimmune encephalomyelitis. In large part, the defective functions of NFATc1(-/-) B cells are caused by decreased BCR-induced Ca(2+) flux and calcineurin (Cn) activation. By affecting CD22, Rcan1, CnA, and NFATc1/alphaA expression, NFATc1 controls the Ca(2+)-dependent Cn-NFAT signaling network and, thereby, the fate of splenic B cells upon BCR stimulation. |
