Abstract

Immunoglobulin E (IgE) is pathogenic in allergic diseases such as asthma, allergic rhinitis, atopic dermatitis, and food allergy. Recent studies using genetically modified IgE reporter mice indicate that the majority of serum IgE in mice is produced by short-lived IgE plasma cells, with minor contributions from long-lived IgE plasma cells, and implicate IgG1 and IgE memory B cells as potential sources of IgE memory. Clinical studies using antibodies against IL-13 or the IL-4 and IL-13 receptor subunit IL-4Rα, as well as an antibody against the M1 prime domain of human membrane IgE, indicate that, similar to mice, a proportion of IgE in humans is derived from ongoing IgE immune responses and short-lived plasma cells. Targeting IgE production may lead to new therapies for the treatment of allergic diseases.

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