Pathogen-specific antibody responses need to be tightly regulated to generate protective but limit self-reactive immune responses. While loss of humoral tolerance has been associated with microbial infections, the pathways involved in balancing protective versus autoreactive antibody responses in humans are incompletely understood. Studies in classical mouse model systems have provided evidence that balancing of immune responses through inhibitory receptors is an important quality control checkpoint. Genetic differences between inbred mouse models and the outbred human population and allelic receptor variants not present in mice; however, argue for caution when directly translating these findings to the human system. By studying Borrelia burgdorferi infection in humanized mice reconstituted with human hematopoietic stem cells from donors homozygous for a functional or a non-functional FcγRIIb allele, we show that the human inhibitory FcγRIIb is a critical checkpoint balancing protective and autoreactive immune responses, linking infection with induction of autoimmunity in the human immune system.

中文翻译：

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人 Fcγ 受体 IIb 调节莱姆关节炎中病原体特异性与自身反应性抗体反应

需要严格调节病原体特异性抗体反应以产生保护性但限制自身反应性免疫反应。虽然体液耐受性的丧失与微生物感染有关，但人们尚未完全了解平衡保护性与自身反应性抗体反应的途径。对经典小鼠模型系统的研究提供的证据表明，通过抑制性受体平衡免疫反应是一个重要的质量控制检查点。近交小鼠模型与远交人群和小鼠中不存在的等位基因受体变体之间的遗传差异；然而，在将这些发现直接转化为人类系统时，应谨慎行事。