Clinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK), University Hospital Tübingen, Tübingen, Germany.
Clinical Collaboration Unit Translational Immunology, German Cancer Consortium (DKTK), University Hospital Tübingen, Tübingen, Germany.
Cell Immunol. 2020 Mar;349:104048. doi: 10.1016/j.cellimm.2020.104048. Epub 2020 Jan 28.
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.
NFAT2 活性在 B 细胞受体信号转导、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不完全清楚。我们证实 NFAT2 缺失导致 B1 B 细胞发育受损，这一发现支持了我们的观点，即在 NFAT2 缺陷小鼠的骨髓和脾脏中，B1 祖细胞数量有限。此外，我们首次表明，NFAT2 的缺失增加了不成熟 B 细胞，特别是过渡性 T2 和 T3 以及成熟滤泡 B 细胞，而边缘区 B 细胞则减少。我们进一步证明 NFAT2 调节 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。总之，本研究对 NFAT2 在周围 B 淋巴细胞发育中的作用进行了广泛分析。
