Journal
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
Volume 134, Issue 6, Pages 1394-+Publisher
MOSBY-ELSEVIER
DOI: 10.1016/j.jaci.2014.06.029
Keywords
Asthma; autoantibodies; IgE; basophil activation; basophil inhibition
Categories
Funding
- Wellcome Trust, United Kingdom [091449/Z/10//24]
- Novartis United Kingdom
- Guy's and St Thomas' Charity
- MRC [G0200485, G0902018, G1100090] Funding Source: UKRI
- Asthma UK [AUK-PG-2013-183, MRC-AsthmaUKCentre] Funding Source: researchfish
- Medical Research Council [G1000758B, G0902018, G1000758, G0200485, G1100090] Funding Source: researchfish
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Background: Naturally occurring IgE-specific IgG autoantibodies have been identified in patients with asthma and other diseases, but their spectrum of functions is poorly understood. Objective: Address the hypothesis that: (i) IgG anti-IgE autoantibodies are detectable in the serum of all subjects but elevated in asthmatic patients regardless of atopic status as compared with controls; (ii) some activate IgE-sensitized basophils; and (iii) some inhibit allergen-induced basophil activation. Methods: IgE-specific IgG autoantibodies were detected and quantified in sera using ELISA. Sera were examined for their ability to activate IgE-sensitized human blood basophils in the presence and absence of allergen using a basophil activation test, and to inhibit allergen binding to specific IgE on a rat basophilic cell line stably expressing human FceRI. Results: IgG autoantibodies binding to both free and Fce RI-bound IgE were detected in patients with atopic and non-atopic asthma, as well as controls. While some were able to activate IgE-sensitised basophils, others inhibited allergen-induced basophil activation, at least partly by inhibiting binding of IgE to specific allergen. Conclusion: Naturally occurring IgG anti-IgE autoantibodies may inhibit, as well as induce, basophil activation. They act in a manner distinct from therapeutic IgG anti-IgE antibodies such as omalizumab. They may at least partly explain why atopic subjects who make allergen-specific IgE never develop clinical symptoms, and why omalizumab therapy is of variable clinical benefit in severe atopic asthma.
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