Korošec Peter, Šilar Mira, Kopač Peter, Eržen Renato, Zidarn Mihaela, Košnik Mitja
University Clinic of Respiratory and Allergic Diseases, Golnik, Slovenia.
Int Arch Allergy Immunol. 2016;171(2):89-101. doi: 10.1159/000452102. Epub 2016 Dec 2.
We sought to determine whether basophil-allergen sensitivity could be transferred to donor basophils by passive IgE sensitisation in allergic rhinitis and anaphylactic Hymenoptera venom hypersensitivity.
We studied 15 wasp venom-, 19 grass pollen- and 2 house dust mite-allergic patients, 2 healthy donors, and 8 wasp venom-allergic donors. In all subjects, we first evaluated the initial basophil response to wasp venom, grass pollen, or house dust mite allergen. Donor basophils were then stripped, sensitised with the different patients' serum IgE, and challenged with the corresponding allergen. The CD63 response of donor basophils was then compared with initial basophil responses.
In wasp venom-allergic subjects, the IgE transfer did not reflect the initial basophil-allergen sensitivity, because the venom IgE of subjects with high or low basophil sensitivity induced comparable responsiveness in healthy donor basophils. Furthermore, vice versa, when we sensitised the donor basophils of wasp venom-allergic individuals with different wasp venom or house dust mite IgE, we demonstrated that their response was predictable by their initial basophil allergen sensitivity. In the rhinitis allergy model, the IgE transfer correlated with the patients' initial basophil responsiveness because the grass pollen IgE of the subjects with high basophil allergen sensitivity induced significantly higher responsiveness of donor basophils than the IgE of subjects with initially low basophil allergen sensitivity.
Our results suggest that basophil allergen sensitivity evaluated by flow-cytometric CD63 analysis depends on two distinct contribution factors. In anaphylactic Hymenoptera allergy, the major factor was intrinsic cellular sensitivity, whereas in pollen allergy, the major factor was allergen-specific IgE on the cell surface.
我们试图确定在过敏性鼻炎和过敏性膜翅目毒液超敏反应中，嗜碱性粒细胞 - 过敏原敏感性是否可通过被动IgE致敏转移至供体嗜碱性粒细胞。
我们研究了15名对黄蜂毒液、19名对草花粉和2名对屋尘螨过敏的患者、2名健康供体以及8名对黄蜂毒液过敏的供体。在所有受试者中，我们首先评估了嗜碱性粒细胞对黄蜂毒液、草花粉或屋尘螨过敏原的初始反应。然后去除供体嗜碱性粒细胞上的原有物质，用不同患者的血清IgE进行致敏，再用相应的过敏原进行激发。随后将供体嗜碱性粒细胞的CD63反应与初始嗜碱性粒细胞反应进行比较。
在对黄蜂毒液过敏的受试者中，IgE转移并未反映初始嗜碱性粒细胞 - 过敏原敏感性，因为高或低嗜碱性粒细胞敏感性受试者的毒液IgE在健康供体嗜碱性粒细胞中诱导出的反应性相当。此外，反之亦然，当我们用不同的黄蜂毒液或屋尘螨IgE对黄蜂毒液过敏个体的供体嗜碱性粒细胞进行致敏时，我们证明其反应可由其初始嗜碱性粒细胞过敏原敏感性预测。在鼻炎过敏模型中，IgE转移与患者的初始嗜碱性粒细胞反应性相关，因为嗜碱性粒细胞过敏原敏感性高的受试者的草花粉IgE比初始嗜碱性粒细胞过敏原敏感性低的受试者的IgE诱导供体嗜碱性粒细胞产生的反应性显著更高。
我们的结果表明，通过流式细胞术CD63分析评估的嗜碱性粒细胞过敏原敏感性取决于两个不同的贡献因素。在过敏性膜翅目过敏中，主要因素是内在细胞敏感性，而在花粉过敏中，主要因素是细胞表面的过敏原特异性IgE。
