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<p>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.</p>

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Seasonal allergen exposure recalls IgE+ plasmablasts to reload allergic effector cells

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月13日

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  • Maria Byazrova,
  • Alla Litovkina,
  • Julia Eckl-Dorna,
  • Huey-Jy Huang,
  • Daria Trifonova,
  • Mohammed Zghaebi,
  • Evgenii Smolnikov,
  • Sabine Flicker,
  • Alfira Romanova,
  • Victoria Stanek,
  • Aldine Tu,
  • Tianchi Jiang,
  • Raffaela Campana,
  • Inna Tulaeva,
  • Susanne Vrtala,
  • Victoria Garib,
  • Olga Elisyutina,
  • Alexander Filatov,
  • Musa Khaitov,
  • Veronika Skvortsova,
  • Rudolf Valenta

摘要

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.