Maria Byazrova, Alla Litovkina, Julia Eckl-Dorna, Huey‐Jy Huang, Daria Trifonova, Mohammed Zghaebi, Evgenii V. Smolnikov, Sabine Flicker, Alfira Romanova, Victoria Stanek, Aldine Tu, Tianchi Jiang, Raffaela Campana, Inna Tulaeva, Susanne Vrtala, Victoria Garib, Olga Elisyutina, Alexander Filatov, Musa Chaitovich Khaitov, Veronika Skvortsova, Rudolf Valenta
Seasonal allergen exposure boosts the production of Immunoglobulin E (IgE) antibodies, leading to allergic diseases affecting more than 30% of the population. However, the cellular mechanisms and pathological consequences of secondary IgE production in humans remain unclear. Here, we demonstrate that IgE⁺ plasmablasts serve as the dominant cellular source responsible for the seasonal amplification of IgE. During birch pollen season, allergen exposure selectively boosts IgE production targeting pre-established conformational epitopes of the major allergen Bet v 1, with no synchronous increase in Bet v 1-specific IgG. Crucially, this plasmablast-derived IgE re-establishes allergen-specific effector cell activation that declines in absence of allergen exposure. Our findings uncover a key role of IgE⁺ plasmablasts in the rapid recall of allergic responses and highlight their potential as a therapeutic target for allergy.