Stringent regulation of IgE antibody production is critical for constraining allergic responses. This review discusses recent advances in understanding cell-intrinsic and extrinsic mechanisms that regulate the genesis and fate of IgE B cells. B cell-intrinsic regulation of IgE is orchestrated by the IgE B Cell Receptor (BCR). Through its antigen-independent signaling and low surface expression, the IgE BCR drives IgE B cells to differentiate into short-lived plasma cells and/or undergo apoptosis, restricting IgE-expressing cells from entering long-lived compartments. The pivotal extrinsic regulators of IgE responses are T follicular helper cells (T_FH). T_FH produce IL-4 and IL-21, which, respectively, are the major activating and inhibitory cytokines for IgE class-switching. Other newly identified T follicular subsets also contribute to IgE regulation. Although IgE responses are normally constrained, recent studies suggest that specific conditions can induce the formation of IgE responses with enhanced affinity or longevity, effectively ‘breaking the rules’ of IgE regulation.

严格调节 IgE 抗体的产生对于限制过敏反应至关重要。本综述讨论了在了解调节 IgE B 细胞发生和命运的细胞内在和外在机制方面的最新进展。IgE 的 B 细胞内在调节由 IgE B 细胞受体 (BCR) 协调。通过其抗原非依赖性信号传导和低表面表达，IgE BCR 驱动 IgE B 细胞分化为短寿命浆细胞和/或经历细胞凋亡，从而限制表达 IgE 的细胞进入长寿命区室。IgE 反应的关键外在调节因子是 T 滤泡辅助细胞 (T _FH )。高飞_{_}产生 IL-4 和 IL-21，它们分别是 IgE 类别转换的主要激活和抑制细胞因子。其他新发现的 T 滤泡亚群也有助于 IgE 调节。尽管 IgE 反应通常受到限制，但最近的研究表明，特定条件可以诱导 IgE 反应的形成，具有增强的亲和力或寿命，有效地“打破了 IgE 调节的规则”。