CD23 can negatively regulate B-cell receptor signaling.
CD23 can negatively regulate B-cell receptor signaling.
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CD23 可以负向调节 B 细胞受体信号传导。
DOI：
10.1038/srep25629
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发表时间：
2016-05-16
影响因子：
4.6
通讯作者：
Song W
中科院分区：
文献类型：
--
作者：
Liu C;Richard K;Wiggins M;Zhu X;Conrad DH;Song W
CD23被认为是免疫球蛋白E和免疫球蛋白抗体反应的负性调节因子。然而，CD23是否在B细胞激活中起作用仍不清楚。我们利用CD23基因敲除(KO)小鼠检测了CD23在不同外周B细胞亚群中的表达，以及CD23表达对B细胞受体(BCR)激活早期事件的影响。我们发现，除了边缘带B细胞外，成熟的滤泡B细胞在经历同型转换和记忆B细胞分化后，显著下调CD23的表面表达水平。在膜相关抗原的刺激下，CD23KO导致接触抗原提呈膜的B细胞面积和bcr聚集量显著增加。这种增强的细胞扩散和BCR聚集伴随着CD23KO B细胞接触区酪氨酸和BTK的磷酸化水平以及F-肌动蛋白和肌动蛋白核促进因子磷酸化的Wiskott Aldrich综合征蛋白水平的增加。这些结果揭示了CD23在缺乏IgE免疫复合体的情况下对BCR信号的负调控作用，并提示CD23通过影响肌动蛋白介导的BCR聚集和B细胞的形态变化而下调BCR信号。
CD23 has been implicated as a negative regulator of IgE and IgG antibody responses. However, whether CD23 has any role in B-cell activation remains unclear. We examined the expression of CD23 in different subsets of peripheral B cells and the impact of CD23 expression on the early events of B-cell receptor (BCR) activation using CD23 knockout (KO) mice. We found that in addition to marginal zone B cells, mature follicular B cells significantly down regulate the surface expression level of CD23 after undergoing isotype switch and memory B-cell differentiation. Upon stimulation with membrane-associated antigen, CD23 KO causes significant increases in the area of B cells contacting the antigen-presenting membrane and the magnitude of BCR clustering. This enhanced cell spreading and BCR clustering is concurrent with increases in the levels of phosphorylation of tyrosine and Btk, as well as the levels of F-actin and phosphorylated Wiskott Aldrich syndrome protein, an actin nucleation promoting factor, in the contract zone of CD23 KO B cells. These results reveal a role of CD23 in the negative regulation of BCR signaling in the absence of IgE immune complex and suggest that CD23 down-regulates BCR signaling by influencing actin-mediated BCR clustering and B-cell morphological changes.
影响因子：
15.3
作者：
Armant, Myriam;Ishihara, Hideki;Rubio, Manuel;Delespesse, Guy;Sarfati, Marika
通讯作者：
Sarfati, Marika