Hyperresponsive B cells in CD22-Deficient mice
Hyperresponsive B cells in CD22-Deficient mice
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DOI：
10.1126/science.274.5288.798
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发表时间：
1996-11-01
期刊：
影响因子：
56.9
通讯作者：
Neuberger, MS
中科院分区：
文献类型：
--
作者：
OKeefe, TL;Williams, GT;Neuberger, MS
CD 22是B淋巴细胞的表面糖蛋白，其在抗原受体交联后在细胞质酪氨酸上迅速磷酸化。来自CD 22基因被破坏的小鼠的脾B细胞被发现对受体信号传导具有高反应性：在较低的配体浓度下获得了增加的钙通量和细胞增殖。小鼠产生增强的免疫应答，具有扩增的腹膜B-1细胞群，并且含有增加的血清自身抗体滴度。因此，CD 22是抗原受体信号传导的负调节剂，其在成熟B细胞阶段表达的开始可用于提高B细胞触发所需的抗原浓度阈值。
CD22 is a surface glycoprotein of B lymphocytes that is rapidly phosphorylated on cytoplasmic tyrosines after antigen receptor cross-linking. Splenic B cells from mice with a disrupted CD22 gene were found to be hyperresponsive lo receptor signaling: Heightened calcium fluxes and cell proliferation were obtained at lower ligand concentrations. The mice gave an augmented immune response, had an expanded peritoneal B-1 cell population, and contained increased serum titers of autoantibody. Thus, CD22 is a negative regulator of antigen receptor signaling whose onset of expression at the mature B cell stage may serve to raise the antigen concentration threshold required for B cell triggering.