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View ResearchExplore the functional plasticity of pathogenic IgE-fated B cell memory. This study reveals that long-lived IgE responses are maintained by an IgG1-dominant memory B cell compartment. By blocking IL-4/IL-13 signaling during antigen re-exposure, researchers demonstrate a shift from a type 2 to a type 1 immune response, suggesting potential therapeutic strategies to reprogram allergen-specific memory B cells and mitigate lifelong allergies.
IgE Memory B Cells and Functional Plasticity
Study reveals IgE memory B cells retain functional plasticity, allowing reprogramming through IL-4/IL-13 blockade.
Impact of IL-4/IL-13 Signaling on B Cells
Blocking IL-4/IL-13 signaling shifts B cell response from type 2 to type 1, preventing IgE production.
Reprogramming Pathogenic IgE-Fated B Cells
Research shows potential to reprogram IgE-fated memory B cells into non-pathogenic IgG2-producing cells.
Germinal Center Responses and Memory B Cells
IL-4/IL-13 blockade enhances germinal center responses, influencing memory B cell fate.
Human and Mouse Models in Allergy Research
Study uses both human and mouse models to demonstrate conserved IL-4/IL-13 signaling in maintaining allergic memory.
Implications for Allergy Treatments
Findings suggest new therapeutic strategies for treating allergies by reprogramming B cell responses.
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