Siglec-G Regulates B1 Cell Survival and Selection
Siglec-G Regulates B1 Cell Survival and Selection
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DOI：
10.4049/jimmunol.1001792
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发表时间：
2010-09-15
影响因子：
4.4
通讯作者：
Nitschke, Lars
中科院分区：
文献类型：
--
作者：
Jellusova, Julia;Dueber, Sandra;Nitschke, Lars
Siglec-G是B1a细胞中BCR介导的信号转导的负调控因子。在Siglec-G缺乏的小鼠中，这种B细胞的数量高度增加，但这种增长的机制到目前为止还不清楚。在这项研究中，我们证明了Siglecg(-/-)B1a细胞表现出较低的自发凋亡水平和较长的寿命。从机制上讲，Siglec-G缺陷B1a细胞中转录因子NFATc1的高表达可能是细胞凋亡率降低的原因。有趣的是，Siglecg(-/-)B1a细胞与野生型B1a细胞相比，表现出不同的BCR谱系。由于Siglecg(-/-)B1a细胞免疫球蛋白的BCR谱系和VDJ组成更像成人骨髓来源的B细胞产生的抗体，而不是典型的胎肝来源的B1a细胞，这表明Siglec-G缺陷小鼠对B1a细胞群体的选择发生了改变。《免疫学杂志》，2010,185：3277-3284。
Siglec-G is a negative regulator of BCR-mediated signaling in B1a cells. This population of B cells is highly increased in Siglec-G-deficient mice, but the mechanism of this expansion is not known so far. In this study, we demonstrate that Siglecg(-/-) B1a cells show a lower level of spontaneous apoptosis and a prolonged life span. Mechanistically, the lower apoptosis could result from higher expression levels of the transcription factor NFATc1 in Siglec-G-deficient B1a cells. Interestingly, Siglecg(-/-) B1a cells display an altered BCR repertoire compared with wild-type B1a cells. As the BCR repertoire and the VDJ composition of Igs of Siglecg(-/-) B1a cells resembles more the Abs produced by adult bone marrow-derived B cells rather than canonical fetal liver-derived B1a cells, this suggest that the selection into the B1a cell population is altered in Siglec-G-deficient mice. The Journal of Immunology, 2010, 185: 3277-3284.