Department of Women and Children's Health (Paediatric Allergy), Faculty of Life Sciences and Medicine, School of Life Course Sciences, King's College London, London, UK.
Peter Gorer Department of Immunobiology, School of Immunology and Microbial Sciences, King's College London, London, UK.
Pediatr Allergy Immunol. 2021 Oct;32(7):1508-1518. doi: 10.1111/pai.13567. Epub 2021 Jun 30.
Immediate food-allergic reactions are IgE-mediated, but many individuals with detectable allergen-specific IgE do not react to the food. Allergen-specific IgG may interfere with allergen-IgE interaction and/or through intracellular inhibitory signalling to suppress mast cell and basophil response to food allergens. We aimed to understand the role of allergen-specific IgG in food allergy and natural tolerance.
IgG and IgG isotypes specific to peanut, cow's milk and egg were measured using ImmunoCAP and ELISA respectively in samples of children with suspected food allergies. Expression of IgE and IgG and their receptors and expression of activation markers following allergen stimulation were measured on basophils and mast cells by flow cytometry, with and without blockade of FcγRIIα or FcγRIIβ receptors.
The levels of peanut-specific IgG, IgG1, IgG2, IgG3 and IgG4 in ELISA were higher in peanut-allergic than in non-peanut-allergic children. No difference in allergen-specific IgG isotypes was observed between allergic and non-allergic children to milk or egg, except for milk-specific IgG4 that was higher in non-cow's milk-allergic than in cow's milk-allergic children. Basophils and LAD2 cells expressed IgG receptors, but IgG and IgA were not detected on the surface of either cell type and blocking FcγRIIα or FcγRIIβ did not modify basophil or mast cell activation in response to allergen in allergic or tolerant children.
Allergen-specific IgG patterns were distinct in persistent (peanut) versus transient (milk and egg) food allergies. We found no evidence that FcγRIIα or FcγRIIβ receptors affect allergen-induced activation of mast cells and basophils in food allergy or natural tolerance.
速发型食物过敏反应是 IgE 介导的,但许多检测到过敏原特异性 IgE 的人不会对食物产生反应。过敏原特异性 IgG 可能会干扰过敏原-IgE 相互作用和/或通过细胞内抑制信号抑制肥大细胞和嗜碱性粒细胞对食物过敏原的反应。我们旨在了解过敏原特异性 IgG 在食物过敏和天然耐受中的作用。
使用 ImmunoCAP 和 ELISA 分别测量疑似食物过敏儿童样本中针对花生、牛奶和鸡蛋的 IgG 和 IgG 同种型的特异性。通过流式细胞术测量过敏原刺激后嗜碱性粒细胞和肥大细胞中 IgE 和 IgG 及其受体的表达,以及在不阻断 FcγRIIα 或 FcγRIIβ 受体的情况下,测量其激活标志物的表达。
ELISA 中花生特异性 IgG、IgG1、IgG2、IgG3 和 IgG4 的水平在花生过敏儿童中高于非花生过敏儿童。除了非牛奶过敏儿童的牛奶特异性 IgG4 高于牛奶过敏儿童外,牛奶或鸡蛋过敏儿童之间的过敏原特异性 IgG 同种型没有差异。嗜碱性粒细胞和 LAD2 细胞表达 IgG 受体,但在这两种细胞类型的表面均未检测到 IgG 和 IgA,并且阻断 FcγRIIα 或 FcγRIIβ 并未改变过敏或耐受儿童对过敏原的嗜碱性粒细胞或肥大细胞的激活。
持续性(花生)与短暂性(牛奶和鸡蛋)食物过敏之间的过敏原特异性 IgG 模式明显不同。我们没有发现 FcγRIIα 或 FcγRIIβ 受体影响食物过敏或天然耐受中过敏原诱导的肥大细胞和嗜碱性粒细胞激活的证据。