Characterization of the B lymphocyte populations in Lyn-deficient mice and the role of Lyn in signal initiation and down-regulation
Characterization of the B lymphocyte populations in Lyn-deficient mice and the role of Lyn in signal initiation and down-regulation
复制标题
DOI：
10.1016/s1074-7613(00)80511-7
复制
发表时间：
1997-07-01
期刊：
影响因子：
32.4
通讯作者：
Lowell, CA
中科院分区：
文献类型：
--
作者：
Chan, VWF;Meng, FY;Lowell, CA
产生Lyn缺陷小鼠以分析林恩在B细胞抗原受体（BCR）信号传导中的作用。这些小鼠的外周B细胞数量减少，未成熟细胞比例更大，更新率高于正常。老年林恩（-/-）小鼠出现脾肿大，产生自身抗体，并具有B1谱系B淋巴母细胞的扩增群体。来自年轻林恩（-/-）小鼠的脾B细胞启动了早期BCR信号传导事件，尽管是以延迟的方式。出乎意料的是，林恩（-/-）B细胞表现出增强的MAP激酶活化和对BCR接合的增殖反应增加。用完整的和F（ab '）（2）抗IgM刺激林恩（-/-）B细胞，发现至少两种负调节BCR信号传导的机制存在缺陷，其中一种机制涉及Fc γ RIIb 1。
Lyn-deficient mice were generated to analyze the role of Lyn in B cell antigen receptor (BCR) signaling. These mice had a reduced number of peripheral B cells with a greater proportion of immature cells and a higher than normal turnover rate. Aged lyn(-/-) mice developed splenomegaly, produced autoantibodies, and had an expanded population of B lymphoblasts of the B1 lineage. Splenic B cells from young lyn(-/-) mice initiated early BCR signaling events, although in a delayed fashion. Unexpectedly, lyn(-/-) B cells exhibited an enhanced MAP kinase activation and an increased proliferative response to BCR engagement. Stimulation of lyn(-/-) B cells with intact and F(ab')(2) anti-IgM revealed defects in at least two mechanisms that negatively regulate BCR signaling, one of which involves Fc gamma RIIb1.