B-cell novel protein 1 (BCNP1) has recently been identified as a new B-cell receptor (BCR) signaling molecule but its physiological function remains unknown. Here, we demonstrate that mice deficient in BCNP1 exhibit impaired B-cell maturation and a reduction of B-1a cells. BCNP1-deficient spleen B cells show enhanced survival, proliferation and Ca2+ influx in response to BCR cross-linking as compared with wild-type spleen B cells. Consistently, mutant B cells show elevated phosphorylation of SYK, B-cell linker protein (BLNK) and PLCγ2 upon BCR cross-linking. In vivo, BCNP1-deficient mice exhibit enhanced humoral immune responses to T-independent and T-dependent antigens. Moreover, aged mutant mice contain elevated levels of serum IgM and IgG3 antibodies and exhibit polyclonal and monoclonal B-cell expansion in lymphoid organs. These results reveal distinct roles for BCNP1 in B-cell development, activation and homeostasis.

中文翻译：

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BCNP1在B细胞发育和激活中的独特作用。

B细胞新蛋白1（BCNP1）最近已被确定为一种新的B细胞受体（BCR）信号分子，但其生理功能仍然未知。在这里，我们证明缺乏BCNP1的小鼠表现出受损的B细胞成熟和B-1a细胞减少。与野生型脾脏B细胞相比，缺乏BCNP1的脾脏B细胞显示出对BCR交联反应增强的存活，增殖和Ca2 +内流。一致地，突变B细胞在BCR交联后显示出SYK，B细胞接头蛋白（BLNK）和PLCγ2的磷酸化升高。在体内，BCNP1缺陷小鼠表现出增强的针对T非依赖性和T非依赖性抗原的体液免疫应答。此外，衰老的突变小鼠血清IgM和IgG3抗体水平升高，并在淋巴器官中表现出多克隆和单克隆B细胞扩增。