Abnormal development and function of B lymphocytes in mice deficient for the signaling adaptor protein SLP-65
Abnormal development and function of B lymphocytes in mice deficient for the signaling adaptor protein SLP-65
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DOI：
10.1016/s1074-7613(00)80130-2
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发表时间：
1999-11-01
期刊：
影响因子：
32.4
通讯作者：
Nielsen, PJ
中科院分区：
文献类型：
--
作者：
Jumaa, H;Wollscheid, B;Nielsen, PJ
在通过B细胞抗原受体（BCR）的信号转导期间，几个信号传导元件通过衔接蛋白SLP-65聚集在一起。我们研究了SLP-65在SLP-65缺陷小鼠中B细胞成熟和功能中的作用。当小鼠存活时，B细胞发育在几个阶段受到影响。SLP-65缺陷小鼠显示骨髓中前B细胞和外周淋巴器官中未成熟B细胞的比例增加。B1 B细胞缺乏。小鼠表现出较低的IgM和IgG 3血清滴度和较差的IgM但正常的IgG免疫应答。突变型B细胞表现出降低的Ca 2+动员和降低的对B细胞有丝分裂原的增殖反应。我们的结论是，白色起着重要的作用，SLP-65并不总是需要从BCR的信号。
During signal transduction through the B cell antigen receptor (BCR), several signaling elements are brought together by the adaptor protein SLP-65. We have investigated the role of SLP-65 in B cell maturation and function in mice deficient for SLP-65. While the mice are viable, B cell development is affected at several stages. SLP-65-deficient mice show increased proportions of pre-B cells in the bone marrow and immature B cells in peripheral lymphoid organs. B1 B cells are lacking. The mice show tower IgM and IgG3 serum titers and poor IgM but normal IgG immune responses. Mutant B cells show reduced Ca2+ mobilization and reduced proliferative responses to B cell mitogens. We conclude that white playing an important role, SLP-65 is not always required for signaling from the BCR.