Lung-resident memory B cells maintain allergic IgE responses in the respiratory tract.

Summary

Using allergen inhalation and reporter mice, the authors show that IgE class switching occurs predominantly within the lung and that lung-resident memory B cells—likely IgG1+ MBCs—maintain airway IgE responses. This identifies a local memory circuit sustaining allergic disease in the respiratory tract.

Key Findings

• Allergen inhalation drives B cell infiltration into lungs and increases airway IgE.
• IgE class switching occurs predominantly within the lung compartment in reporter mice.
• An IgG1-lineage memory B cell population likely sustains local IgE responses in the respiratory tract.

Clinical Implications

Therapies that disrupt lung-resident memory B cell niches or IgG1-to-IgE switching in airway tissues could provide durable control of allergic disease beyond systemic anti-IgE approaches.

Limitations

• Mouse model findings require validation in human airway tissues
• Limited detail on human translational evidence in the abstract

Future Directions

Define human lung-resident B cell subsets maintaining IgE, and test strategies to disrupt local memory niches or block class-switch circuitry to reduce allergic disease relapses.