ArrayExpress Uploader06024unstimulated3h8h16hunstimulated3h8h16hunstimulated3h8h16hunstimulated3h8h16hunstimulated3h8h16hunstimulated3h8h16harrayexpress_sid6Triggering of B cell receptors (BCR) induces a massive synthesis of NFATc1 in splenic B cells. By inactivating the Nfatc1 gene and re-...21464221E-GEOD-21063/profile/8773/arrayexpressuploader124cellclassencephalomyelitisimmunoglobulinDec.12, 2014Falsenfatc1-controls-the-survival-function-and-suppressE-GEOD-21063_A-AFFY-45NFATc1 controls the survival, function and suppressive capacity of B lymphocytes upon B cell receptor stimulationNov.11, 2014Triggering of B cell receptors (BCR) induces a massive synthesis of NFATc1 in splenic B cells. By inactivating the Nfatc1 gene and re-expressing NFATc1 we show that NFATc1 levels are critical for the survival of splenic B cells upon BCR stimulation. NFATc1 ablation led to decreased BCR-induced Ca++ flux and proliferation of splenic B cells, increased apoptosis and suppressed germinal centre formation and immunoglobulin class switch by T cell-independent antigens. By controlling IL-10 synthesis in B cells, NFATc1 supported the proliferation and IL-2 synthesis of T cells in vitro and appeared to contribute to the mild clinical course of Experimental Autoimmune Encephalomyelitis in mice bearing NFATc1-/- B cells. These data indicate NFATc1 as a key factor controlling B cell function. Splenic mice cells were isolated from mice bearing NFATc1 deficient B-cells and from control mice, stimulated with anti-IgM for 0h, 3h, 8h and 16h, respectively and isolated using Milteny beads to enrich the B cell population. This experiment was performed in 3 biological replicates.http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-21063mousehttp://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-21063/samples/