Eeva J, Pelkonen J
Department of Clinical Microbiology, University of Kuopio, Kuopio, FIN-70211, Finland.
Apoptosis. 2004 Sep;9(5):525-31. doi: 10.1023/B:APPT.0000038032.22343.de.
B cell receptor (BCR)-mediated apoptosis plays a key role in the negative selection (deletion) of autoreactive B cells. Mechanisms of BCR-mediated apoptosis have been widely studied in cell lines representing both immature (bone marrow) and mature (germinal center) B cells. However, there is much inconsistency and controversy concerning the possible mechanisms of BCR-mediated apoptosis, which may reflect differences in the origin or the maturational stage of the cell line used. Based on recent studies, collapse of mitochondrial membrane potential (Delta Psi m) seems to be an essential event for BCR-mediated apoptosis in both mature and immature cells. The collapse of Delta Psi m is dependent on the synthesis of new proteins, which are involved in the permeability change of mitochondrial membranes. Mitochondrial dysfunction induces activation of caspases, cysteine proteases, which play a central role in apoptosis. However, instead of caspases, other effector proteases, such as cathepsins or calpains, may also be responsible for the organized destruction of cell components seen during BCR-mediated apoptosis.
B细胞受体（BCR）介导的凋亡在自身反应性B细胞的阴性选择（删除）中起关键作用。BCR介导的凋亡机制已在代表未成熟（骨髓）和成熟（生发中心）B细胞的细胞系中得到广泛研究。然而，关于BCR介导的凋亡的可能机制存在很多不一致和争议，这可能反映了所用细胞系的起源或成熟阶段的差异。基于最近的研究，线粒体膜电位（ΔΨm）的崩溃似乎是成熟和未成熟细胞中BCR介导的凋亡的一个基本事件。ΔΨm的崩溃依赖于新蛋白质的合成，这些新蛋白质参与线粒体膜的通透性变化。线粒体功能障碍诱导半胱天冬酶（一种在凋亡中起核心作用的半胱氨酸蛋白酶）的激活。然而，除了半胱天冬酶外，其他效应蛋白酶，如组织蛋白酶或钙蛋白酶，也可能负责在BCR介导的凋亡过程中看到的细胞成分的有组织破坏。
