CD22 is both a positive and negative regulator of B lymphocyte antigen receptor signal transduction: Altered signaling in CD22-deficient mice
CD22 is both a positive and negative regulator of B lymphocyte antigen receptor signal transduction: Altered signaling in CD22-deficient mice
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DOI：
10.1016/s1074-7613(00)80270-8
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发表时间：
1996-12-01
期刊：
影响因子：
32.4
通讯作者：
Tedder, TF
中科院分区：
文献类型：
--
作者：
Sato, S;Miller, AS;Tedder, TF
抗原受体交联后的 B 细胞活化可以在体外通过连接细胞表面 CD22 来增强，CD22 与 SHP1 蛋白酪氨酸磷酸酶结合。小鼠体内 CD22 的靶向缺失表明，CD22 对静息和抗原刺激的 B 淋巴细胞中的抗原受体信号传导有差异性调节。来自 CD22 缺陷小鼠的细胞表现出细胞表面表型和增强的细胞内钙反应特征，这是长期刺激的 B 细胞的特征，就像在 SHP1 缺陷小鼠中发生的那样。因此，在没有抗原的情况下，CD22 负向调节抗原受体信号传导。然而，通过延长 IgM 交联激活缺乏 CD22 的 B 淋巴细胞会导致适度的 B 细胞增殖，这表明 CD22 在抗原存在下正向调节抗原受体信号传导。
B cell activation following antigen receptor cross-linking can be augmented in vitro by ligation of cell surface CD22, which associates with the SHP1 protein tyrosine phosphatase. The targeted deletion of CD22 in mice demonstrated that CD22 differentially regulates antigen receptor signaling in resting and antigen-stimulated B lymphocytes. a cells from CD22-deficient mice exhibited the cell surface phenotype and augmented intracellular calcium responses characteristic of chronically stimulated B cells, as occurs in SHP1-defective mice. Thus, CD22 negatively regulates antigen receptor signaling in the absence of antigen. However, activation of CD22-deficient B lymphocytes by prolonged IgM cross-linking resulted in modest B cell proliferation, demonstrating that CD22 positively regulates antigen receptor signaling in the presence of antigen.