Bhattacharyya S, Deb J, Patra AK, Duong Anh Thuy Pham , Chen W, Vaeth M, Berberich-Siebelt F, Klein-Hessling S, Lamperti ED, Reifenberg K, Jellusova J, Schweizer A, Nitschke L, Leich E, Rosenwald A, Brunner C, Engelmann S, Bommhardt U, Avots A, Mueller MR, Kondo E, Serfling E (2011)
Publication Status: Published
Publication Type: Journal article
Publication year: 2011
Publisher: ROCKEFELLER UNIV PRESS
Book Volume: 208
Pages Range: 823-839
Journal Issue: 4
DOI: 10.1084/jem.20100945
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/alpha A, 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 IgG31(+) 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 Ca2+ flux and calcineurin (Cn) activation. By affecting CD22, Rcan1, CnA, and NFATc1/alpha A expression, NFATc1 controls the Ca2+-dependent Cn-NFAT signaling network and, thereby, the fate of splenic B cells upon BCR stimulation.
APA:
Bhattacharyya, S., Deb, J., Patra, A.K., Duong Anh Thuy Pham, ., Chen, W., Vaeth, M.,... Serfling, E. (2011). NFATc1 affects mouse splenic B cell function by controlling the calcineurin-NFAT signaling network. Journal of Experimental Medicine, 208(4), 823-839. https://doi.org/10.1084/jem.20100945
MLA:
Bhattacharyya, Sankar, et al. "NFATc1 affects mouse splenic B cell function by controlling the calcineurin-NFAT signaling network." Journal of Experimental Medicine 208.4 (2011): 823-839.
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