Atopy (Allergy) Research Center, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.
Department of Science of Allergy and Inflammation, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.
Cells. 2021 Jul 5;10(7):1697. doi: 10.3390/cells10071697.
The recent emergence of anti-immunoglobulin E (IgE) drugs and their candidates for humans has endorsed the significance of IgE-dependent pathways in allergic disorders. IgE is distributed locally in the tissues or systemically to confer a sensory mechanism in a domain of adaptive immunity to the otherwise innate type of effector cells, namely, mast cells and basophils. Bound on the high-affinity IgE receptor FcεRI, IgE enables fast memory responses against revisiting threats of venoms, parasites, and bacteria. However, the dysregulation of IgE-dependent reactions leads to potentially life-threatening allergic diseases, such as asthma and anaphylaxis. Therefore, reactivity of the IgE sensor is fine-tuned by various IgE-associating molecules. In this review, we discuss the mechanistic basis for how IgE-dependent mast cell activation is regulated by the IgE-associating molecules, including the newly developed therapeutic candidates.
最近出现的抗免疫球蛋白 E(IgE)药物及其在人类中的候选药物证实了 IgE 依赖性途径在过敏疾病中的重要性。IgE 局部分布在组织中或全身分布,赋予适应性免疫的一个领域以感觉机制,而适应性免疫的效应细胞原本是先天类型的,即肥大细胞和嗜碱性粒细胞。IgE 结合到高亲和力 IgE 受体 FcεRI 上,使机体能够对毒液、寄生虫和细菌再次入侵的威胁产生快速的记忆反应。然而,IgE 依赖性反应的失调会导致潜在的危及生命的过敏性疾病,如哮喘和过敏反应。因此,IgE 传感器的反应性由各种 IgE 相关分子进行微调。在这篇综述中,我们讨论了 IgE 依赖性肥大细胞激活如何受到 IgE 相关分子(包括新开发的治疗候选物)调节的机制基础。