Abstract

Abstract IgE-mediated allergies depend on the continuous production of allergen-specific IgE to maintain allergic sensitization. While IgE+ plasma cells are the primary source of this IgE, IgE+ plasmablasts can provide a snapshot in peripheral blood of the current response to allergen. We developed a novel approach to characterize IgE+ plasmablasts in peripheral blood and determined the relationship between allergen exposure, IgE+ plasmablasts and clinical disease. We used a unique large animal model of naturally occurring allergy, equine Culicoides hypersensitivity, which allowed all individuals to have similar timing and frequency of allergen exposure and allowed longitudinal collection of samples from the same allergic and healthy individuals over time. We found that peripheral IgE+ plasmablasts spontaneously secrete IgE, express high levels of the IgE receptor CD23 on their surface, and positively correlate with clinical disease severity. In conclusion, IgE+ plasmablasts are critical in the mechanism of allergy through IgE secretion and serve as a quantitative biomarker of allergic disease development and severity. This work was supported by the Harry M. Zweig Memorial Fund for Equine Research at Cornell University; the USDA/NIFA [#2005-01812, #2015-67015-23072, and #2019-67015-29833]; and National Institutes of Health [#1S10RR025502 through Cornell University’s Biotechnology Resource Center].

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