Kurosaki T
Department of Molecular Genetics, Kansai Medical University, Moriguchi, Japan.
Annu Rev Immunol. 1999;17:555-92. doi: 10.1146/annurev.immunol.17.1.555.
In B lymphocytes, a signaling complex that contributes to cell fate decisions is the B cell antigen receptor (BCR). Data from knockout experiments in cell lines and mice have revealed distinct functions for the intracellular protein tyrosine kinases (Lyn, Syk, Btk) in BCR signaling and B cell development. Combinations of intracellular signaling pathways downstream of these PTKs determine the quality and quantity of BCR signaling. For example, concerted actions of the PLC-gamma 2 and PI3-K pathways are required for proper calcium responses. Similarly, the regulation of ERK and JNK responses involves both PLC-gamma 2 and GTPases pathways. Since the immune response in vivo is regulated by alteration of these signaling outcomes, achieving a precise understanding of intracellular molecular events leading to B lymphocyte proliferation, deletion, anergy, receptor editing, and survival still remains a challenge for the future.
在B淋巴细胞中，一种有助于细胞命运决定的信号复合物是B细胞抗原受体（BCR）。来自细胞系和小鼠基因敲除实验的数据揭示了细胞内蛋白酪氨酸激酶（Lyn、Syk、Btk）在BCR信号传导和B细胞发育中的不同功能。这些蛋白酪氨酸激酶下游的细胞内信号通路组合决定了BCR信号传导的质量和数量。例如，PLC-γ2和PI3-K途径的协同作用是产生适当钙反应所必需的。同样，ERK和JNK反应的调节涉及PLC-γ2和GTP酶途径。由于体内免疫反应受这些信号转导结果改变的调节，因此精确了解导致B淋巴细胞增殖、缺失、无反应性、受体编辑和存活的细胞内分子事件仍是未来面临的一项挑战。
