The uniqueness of each B cell lies in the structural diversity of the B-cell antigen receptor allowing the virtually limitless recognition of antigens, a necessity to protect individuals against a range of challenges. B-cell development and response to stimulation are exquisitely regulated by a group of cell surface receptors modulating various signaling cascades and their associated genetic programs. The effects of these signaling pathways in optimal antibody-mediated immunity or the aberrant promotion of immune pathologies have been intensely researched in the past in young individuals. In contrast, we are only beginning to understand the contribution of these pathways to the changes in B cells of old organisms. Thus, critical transcription factors such as E2A and STAT5 show differential expression or activity between young and old B cells. As a result, B-cell physiology appears altered, and antibody production is impaired. Here, we discuss selected phenotypic changes during B-cell aging and attempt to relate them to alterations of molecular mechanisms.

每个B细胞的独特性在于B细胞抗原受体的结构多样性，从而使抗原几乎可以无限地被识别，这是保护个人免受一系列挑战的必要条件。B细胞发育和对刺激的反应受到一组调节各种信号传导级联及其相关遗传程序的细胞表面受体的调控。这些信号通路在最佳抗体介导的免疫或免疫病理异常促进中的作用过去已在年轻人中进行了深入研究。相反，我们才刚刚开始了解这些途径对旧生物的B细胞变化的贡献。因此，关键的转录因子，例如E2A和STAT5，在年轻和老B细胞之间显示出不同的表达或活性。结果，B细胞生理学似乎改变，并且抗体产生受损。在这里，我们讨论了B细胞衰老过程中选定的表型变化，并试图将其与分子机制的改变联系起来。