Siglec-G is a B1 cell-inhibitory receptor that controls expansion and calcium signaling of the B1 cell population
Siglec-G is a B1 cell-inhibitory receptor that controls expansion and calcium signaling of the B1 cell population
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DOI：
10.1038/ni1480
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发表时间：
2007-07-01
影响因子：
30.5
通讯作者：
Nitschke, Lars
中科院分区：
文献类型：
--
作者：
Hoffmann, Anja;Kerr, Sheena;Nitschke, Lars
B1细胞是产生天然抗体和抗菌免疫球蛋白应答的重要细胞群。在这里，我们确定了小鼠蛋白Siglec-G作为B1细胞抑制受体。Siglec-G以B细胞限制性方式表达，大量存在于B1细胞中。当过表达时，Siglec-G抑制B细胞受体介导的钙信号传导。Siglec-G缺陷小鼠的B1 a细胞群大量扩增，这在发育早期就开始了，是B细胞固有的。Siglec-G缺陷小鼠具有更高的天然IgM抗体滴度，但不具有更高的IgG自身抗体滴度。Siglec-G缺陷的B1细胞显示出强烈增强的钙信号传导。我们的研究结果表明，Siglec-G依赖的负调控存在于B1细胞中，这可能解释了B1细胞的自然沉默的信号反应。
B1 cells are an important cell population for the production of natural antibodies and for antibacterial immunoglobulin responses. Here we identified the mouse protein Siglec-G as a B1 cell inhibitory receptor. Siglec-G was expressed in a B cell restricted way, with large amounts present in B1 cells. When overexpressed, Siglec-G inhibited B cell receptor-mediated calcium signaling. Siglec-G-deficient mice had massive expansion of the B1a cell population, which began early in development and was B cell intrinsic. Siglec-G- deficient mice had higher titers of natural IgM antibodies but not a higher penetrance of IgG autoantibodies. Siglec-G-deficient B1 cells showed a strongly enhanced calcium signaling. Our results demonstrate that Siglec-G-dependent negative regulation exists in B1 cells, which may explain the naturally muted signaling response of B1 cells.