Division of Human Genetics Cincinnati Children's Hospital Medical Center, Suite R-1007, MLC 7016, 3333 Burnet Avenue, Cincinnati, OH, 45229, USA,
Curr Allergy Asthma Rep. 2013 Dec;13(6):596-606. doi: 10.1007/s11882-013-0387-3.
Allergy and asthma are triggered primarily by the binding of allergen-specific immunoglobulin E (IgE)-allergen complexes to their receptors, recognition of the allergens by antigen-presenting cells, and allergen presentation to the T cells. These events lead to mucus secretions, runny nose, itchy eyes, sneezing, airway hyperresponsiveness, and nasal congestion. Complement 5a (C5a) has emerged as a central molecule that mediates these allergic reactions. Many allergens and allergen-specific IgG immune complexes (IgG-ICs) cause complement activation and C5a generation. C5a interaction with its receptor (C5aR) leads to the infiltration and activation of several immunologic cell types and the secretion of pathogenic inflammatory and proinflammatory mediators. However, IgG1-IC binding to the IgG inhibitory Fc gamma receptor (FcγRIIB) suppresses C5aR-mediated inflammatory signaling and, hence, may reduce the inflammatory immune responses through this FcγRIIB-mediated pathway. Reviews of the IgG1-IC interactions with C5a-mediated inflammatory immune responses suggest that IgG1-IC-C5a inhibitory therapy may reduce inflammation in allergic diseases.
过敏和哮喘主要是由过敏原特异性免疫球蛋白 E（IgE）-过敏原复合物与其受体结合、抗原呈递细胞识别过敏原以及过敏原呈递给 T 细胞引发的。这些事件导致黏液分泌、流鼻涕、眼睛发痒、打喷嚏、气道高反应性和鼻塞。补体 5a（C5a）已成为介导这些过敏反应的中心分子。许多过敏原和过敏原特异性 IgG 免疫复合物（IgG-IC）引起补体激活和 C5a 的产生。C5a 与其受体（C5aR）的相互作用导致几种免疫细胞类型的浸润和激活，以及致病炎症和促炎介质的分泌。然而，IgG1-IC 与 IgG 抑制性 Fc 受体（FcγRIIB）结合会抑制 C5aR 介导的炎症信号转导，因此，通过这种 FcγRIIB 介导的途径，可能会减少炎症免疫反应。对 IgG1-IC 与 C5a 介导的炎症免疫反应的综述表明，IgG1-IC-C5a 抑制治疗可能会减轻过敏疾病中的炎症。
