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B细胞表面抗原受体(BCR)与其抗原或其它配体(如anti-μMcAb)的结合启动了B细胞的活化。BCR交联后,首先在其ITAM序列部位发生酪氨酸磷酸化,从而富集并激活Src家族蛋白质酪氨酸激酶(PTK),进而Src家族PTK将SykPTK等的酪氨酸磷酸化而活化,使信号传递下去。在此过程中,还有FcγRⅡb和CD22等分子通过富集蛋白质酪氨酸磷酸酶PTP1C活化信号进行负调控。本文对此BCR信号转导早期阶段的主要途径及其调控机理进行综述。
B cell surface antigen receptor (BCR) binding to its antigen or other ligands (such as anti-μMcAb) initiates the activation of B cells. After BCR cross-linking, tyrosine phosphorylation occurs first in its ITAM sequence site, thereby enriching and activating the Src family protein tyrosine kinase (PTK). Furthermore, Src family PTK phosphorylates and activates tyrosine such as SykPTK, Let the signal pass down. In the process, other molecules such as FcγRⅡb and CD22 are negatively regulated by the enrichment of protein tyrosine phosphatase PTP1C activation signal. This review summarizes the main pathway of BCR signal transduction in the early stage and its regulatory mechanism.