腺样体扁桃体肥大相关B细胞免疫活化调控机制的研究进展

Advancements in understanding the regulatory mechanism of B-cell immune activation associated with adenotonsillar hypertrophy

摘要:

B细胞通过其表面分布的 B细胞受体 （BCR） 识别外界抗原，是机体产生保护性抗体与免疫记忆的关键步骤。 B细胞免疫活化调控与诸多上呼吸道疾病是密切相关的。儿童常见疾病腺样体扁桃体肥大 （ATH），其特征性病理本质为淋巴滤泡的增生，但其确切机制尚未明确。本文综述静息态下维持B细胞存活的BCR滋养信号研究，阐述了B细胞免疫活化及产生快速高效免疫记忆的调控机制，尤其是活化早期分子事件，强调mIgG-tail对记忆性抗体应答的相关作用。B细胞活化调控过程出现异常可破坏免疫稳态平衡，导致疾病的发生。本文总结了B细胞免疫活化调控与ATH的机制关联，尝试探讨信号转导通路失调或突变对ATH的可能影响。旨在深入理解ATH的致病机理，以期挖掘潜在研究突破口，寻找ATH新的诊疗靶点。

Abstract:

B cells play a crucial role in recognizing external antigens through their surface B cell receptor (BCR), essential for generating protective antibodies and immune memory. Regulation of B cell immune activation is closely linked to various upper respiratory tract diseases. Adenoid hypertrophy (ATH), a common childhood condition, is characterized by lymphoid follicular hyperplasia, yet its exact mechanisms remain elusive. This review consolidates research on BCR trophic signaling that sustains B cell viability in resting state. It clarifies the regulatory mechanisms governing B cell immune activation and the establishment of rapid, effective immune memory, with a specific focus on early molecular activation events and the pivotal role of mIgG-tail in memory antibody responses. Dysregulation of B cell activation processes can disrupt immune balance, potentially precipitating disease. This synthesis explores the connection between regulation of B cell activation and ATH pathogenesis, examining the potential impacts of signaling pathway dysregulation or mutations on ATH. The review aims to enhance understanding of the disease mechanisms underlying ATH, with the goal of identifying new diagnostic and therapeutic targets for this condition.