锡克
B细胞
断点群集区域
B细胞受体
B-1电池
细胞生物学
生物
免疫系统
幼稚B细胞
多克隆B细胞反应
脾脏
分子生物学
磷酸化
T细胞
信号转导
抗体
受体
免疫学
抗原提呈细胞
酪氨酸激酶
生物化学
作者
Rongjian Hong,Nannan Lai,Ermeng Xiong,Rika Ouchida,Jiping Sun,Yang Zhou,Yue Tang,Masaki Hikida,Takeshi Tsubata,Masatoshi Tagawa,Yan-Qing Wang,Ji‐Yang Wang
标识
DOI:10.1093/intimm/dxz055
摘要
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.
科研通智能强力驱动
Strongly Powered by AbleSci AI