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B Cell Hyperresponsiveness and Expansion of Mature Follicular B Cells but Not of Marginal Zone B Cells in NFATc2/c3 Double-Deficient Mice¹

Devapriya Nandini Samanta^*, Alois Palmetshofer^*, Dragan Marinkovic^2,, Thomas Wirth, Edgar Serfling^3,4,* and Lars Nitschke^3,4,

^* Department of Molecular Pathology, Institute of Pathology, and Institute for Virology and Immunobiology, University of Würzburg, Würzburg, Germany; and Department of Physiological Chemistry, University of Ulm, Ulm, Germany

Marginal zone (MZ) B cells and peritoneal B-1 cells provide a first defense system of thymus-independent Ab responses against foreign pathogens and therefore share a number of functional properties. Recently, development of B-1a cells was shown to be controlled by the transcription factor NFATc1. We show here that mice deficient for NFATc2 and c3 display a distinct lower representation of MZ B cells, which is correlated with a reduced capturing of trinitrophenyl-Ficoll. In contrast, mature follicular B cells from NFATc2/c3^–/– mice are strongly increased in number. NFATc2/c3^–/– B cells exhibit a marked increase in BCR-induced intracellular Ca²⁺ mobilization and proliferation. However, trinitrophenyl-Ficoll-specific IgM and IgG3 responses of NFATc2/c3-deficient mice are intact, and chimeric mice reconstituted with NFATc2/3-deficient B cells show a normal number of MZ B cells and normal BCR responses. These observations suggest that the strongly elevated Th2 cytokine milieu in NFATc2/c3-deficient mice leads to a hyperactivation of mature, follicular B cells, whereas MZ B cells are less responsive to these signals.

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