Type I hypersensitivity, also known as classical allergy, is mediated via allergen‐specific IgE antibodies bound to type I FcR (FcεRI) on the surface of mast cells and basophils upon cross‐linking by allergens. This IgE‐mediated cellular activation may be blocked by allergen‐specific IgG through multiple mechanisms, including direct neutralization of the allergen or engagement of the inhibitory receptor FcγRIIb which blocks IgE signal transduction. In addition, co‐engagement of FcεRI and FcγRIIb by IgE‐IgG‐allergen immune complexes causes down regulation of receptor‐bound IgE, resulting in desensitization of the cells. Both, activation of FcεRI by allergen‐specific IgE and engagement of FcγRIIb by allergen‐specific IgG are driven by allergen‐binding. Here we delineate the distinct roles of antibody affinity versus avidity in driving these processes and discuss the role of IgG subclasses in inhibiting basophil and mast cell activation.

中文翻译：

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抗体亲和力和亲和力在 IgE 介导的过敏反应中的作用


I 型超敏反应，也称为经典过敏，是通过变应原交联后与肥大细胞和嗜碱性粒细胞表面的 I 型 FcR （FcεRI） 结合的变应原特异性 IgE 抗体介导的。这种 IgE 介导的细胞激活可能通过多种机制被过敏原特异性 IgG 阻断，包括直接中和过敏原或阻断 IgE 信号转导的抑制性受体 FcγRIIb 的参与。此外，IgE-IgG-过敏原免疫复合物共结合 FcεRI 和 FcγRIIb 导致受体结合的 IgE 下调，导致细胞脱敏。过敏原特异性 IgE 对 FcεRI 的激活和过敏原特异性 IgG 对 FcγRIIb 的结合都是由过敏原结合驱动的。在这里，我们描述了抗体亲和力与亲和力在驱动这些过程中的不同作用，并讨论了 IgG 亚类在抑制嗜碱性粒细胞和肥大细胞活化中的作用。