Lapitan Christian, Zhang William R, Guo Beichu, Daniels-Wells Tracy R, Penichet Manuel L, Zhang Ke
Allerdia Inc., Torrance, CA, United States.
Division of Dermatology, Department of Medicine, David Geffen School of Medicine at UCLA, University of California, Los Angeles, Los Angeles, CA, United States.
Immunohorizons. 2025 May 30;9(7). doi: 10.1093/immhor/vlaf018.
IgE cross-reactivity among peanut allergens is controversial, and allergenicity of peanut allergens other than Arachis hypogaea 2 [Ara h 2] remains to be elucidated. We investigated the origins of peanut IgE cross-reactivity using Western blotting, and allergenicity of peanut allergens employing a passive cutaneous anaphylaxis model. Peanut allergic IgE bound to a large swath of peanut proteins including Ara h 2, Ara h 1, Ara h 3, and Ara h 6. IgE cross-reactivity among peanut allergens could be inhibited by recombinant Ara h 2. Affinity-purified Ara h 2 IgE reconstituted broad IgE binding patterns to Ara h 1, Ara h 3, and Ara h 6 in addition to Ara h 2. Monoclonal human IgE and mouse IgG against peanut allergen component variably bound to other peanut allergen components. Ara h 2 and Ara h 6 could trigger Ara h 2 IgE-mediated peanut allergic reactivity, whereas Ara h 1 and Ara h 3 failed to do so. Ara h 1 IgE was incapable of mediating Ara h 1-triggered allergic reaction. These results revealed that Ara h 2 IgE was the origin of IgE cross-reactivity, and Ara h 2 IgE-mediated peanut allergic reactivity triggered by Ara h 2 and Ara h 6. Ara h 1 and Ara h 3 did not display detectable allergenicity. These results indicated that Ara h 2 IgE appeared to be the "master" responsible for IgE cross-reactivity among peanut allergens and might be the only IgE responsible for allergic reactivity in peanut allergy.
花生过敏原之间的IgE交叉反应性存在争议，除了花生过敏原2 [Ara h 2]之外的花生过敏原的致敏性仍有待阐明。我们使用蛋白质印迹法研究了花生IgE交叉反应性的起源，并采用被动皮肤过敏反应模型研究了花生过敏原的致敏性。花生过敏IgE与包括Ara h 2、Ara h 1、Ara h 3和Ara h 6在内的大量花生蛋白结合。重组Ara h 2可抑制花生过敏原之间的IgE交叉反应性。亲和纯化的Ara h 2 IgE除了与Ara h 2结合外，还重建了与Ara h 1、Ara h 3和Ara h 6广泛的IgE结合模式。针对花生过敏原成分的单克隆人IgE和小鼠IgG与其他花生过敏原成分的结合各不相同。Ara h 2和Ara h 6可引发Ara h 2 IgE介导的花生过敏反应，而Ara h 1和Ara h 3则不能。Ara h 1 IgE无法介导Ara h 1引发的过敏反应。这些结果表明，Ara h 2 IgE是IgE交叉反应性的起源，并且Ara h 2 IgE介导了由Ara h 2和Ara h 6引发的花生过敏反应。Ara h 1和Ara h 3未显示出可检测到的致敏性。这些结果表明，Ara h 2 IgE似乎是花生过敏原之间IgE交叉反应性的“主导者”，并且可能是花生过敏中唯一负责过敏反应的IgE。
