NFAT2 activity was shown to be of critical importance in B cell receptor signaling, development and proliferation; however its role in B cell development in the periphery is still not completely understood. We confirmed that NFAT2 deletion leads to impaired B1 B cell development, supported by our finding of limited B1 progenitors in the bone marrow and spleen of NFAT2 deficient mice. Moreover, we show for the first time that loss of NFAT2 increases immature B cells in particular transitional T2 and T3 as well as mature follicular B cells while marginal zone B cells are decreased. We further demonstrate that NFAT2 regulates the expression of B220, CD23, CD38, IgM/IgD and ZAP70 in murine B cells. In vivo analyses revealed decreased proliferation and increased apoptosis of NFAT2 deficient B cells. In summary, this study provides an extensive analysis of the role of NFAT2 in peripheral B lymphocyte development.

中文翻译：

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NFAT2（NFATc1）的遗传损失会损害B1和B2 B细胞的B细胞发育。

NFAT2活性在B细胞受体信号传导，发育和增殖中至关重要。然而，其在周围B细胞发育中的作用仍未完全了解。我们证实了NFAT2缺失会导致B1 B细胞发育受损，这是由我们在NFAT2缺陷小鼠的骨髓和脾脏中有限的B1祖细胞的发现所支持的。此外，我们首次显示NFAT2的缺失会增加未成熟的B细胞，特别是过渡性T2和T3以及成熟的卵泡B细胞，而边缘B区细胞则减少。我们进一步证明，NFAT2调节鼠B细胞中B220，CD23，CD38，IgM / IgD和ZAP70的表达。体内分析显示NFAT2缺陷B细胞的增殖减少和凋亡增加。综上所述，