Signal transduction through Vav-2 participates in humoral immune responses and B cell maturation
Signal transduction through Vav-2 participates in humoral immune responses and B cell maturation
复制标题
DOI：
10.1038/88748
复制
发表时间：
2001-06-01
影响因子：
30.5
通讯作者：
Turner, M
中科院分区：
文献类型：
--
作者：
Doody, GM;Bell, SE;Turner, M
在缺乏鸟嘌呤核苷酸交换因子Vav-2的小鼠中，B和T淋巴细胞发育正常，但对II型胸腺非依赖性抗原的免疫应答以及对胸腺依赖性（TD）抗原的初级应答是缺陷的。缺乏Vav-2的小鼠在转换免疫球蛋白类别、形成生殖中心和产生对TD抗原的二次免疫应答的能力方面也有缺陷。缺乏Vav-1和Vav-2的小鼠含有减少数量的B淋巴细胞，并在成熟B细胞的发育中显示出成熟阻滞。来自Vav-1（-/-）Vav-2（-/-）小鼠的B细胞在增殖和钙释放方面对抗原受体触发的反应都很差。这些研究表明Vav-2在体液免疫应答和B细胞成熟中的重要性。
B and T lymphocytes develop normally in mice lacking the guanine nucleotide exchange factor Vav-2, However, the immune responses to type II thymus-independent antigen as well as the primary response to thymus-dependent (TD) antigen are defective. Vav-2-deficient mice are also defective in their ability to switch immunoglobulin class, form germinal centers and generate secondary immune responses to TD antigens, Mice lacking both Vav-1 and Vav-2 contain reduced numbers of B lymphocytes and display a maturational block in the development of mature B cells. B cells from Vav-1(-/-)Vav-2(-/-) mice respond poorly to antigen receptor triggering, both in terms of proliferation and calcium release. These studies show the importance of Vav-2 in humoral immune responses and B cell maturation.