B cell development and longevity of IgE plasma cells

Among the five antibody isotypes, immunoglobulin E (IgE) is unique in both its biological potency and clinical associations. Secreted by a specialized subset of plasma cells, IgE plays a critical role in host defense against helminths and other parasitic infections. Its effector functions are mediated through two main mechanisms: (1) opsonization of parasite surfaces, which enables eosinophil recognition of the Fc region of IgE, leading to eosinophil degranulation and parasite destruction; and (2) potent activation of mast cells and basophils through high-affinity binding to FcεRI. Among all immunoglobulin (Ig) isotypes, IgE exhibits the strongest affinity for FcεRI on mast cells, underscoring its ability to trigger robust immune activation. However, despite the IgE signaling axis providing protection against parasites, it is also a central driver of allergic pathology, with elevated systemic IgE being strongly implicated in atopic diseases such as allergic rhinitis, asthma, and eczema. Emerging research has refined our understanding of the IgE signaling axis, revealing the existence of two distinct subsets of IgE-secreting plasma cells: short-lived (SLPC) and long-lived (LLPC). This distinction has profound implications: SLPC are responsible for acute reactions, whereas LLPC are responsible for chronic IgE-mediated inflammatory conditions. This review aims to synthesize current knowledge on the development and regulation of IgE-producing plasma cells, and to explore how their longevity may influence the pathogenesis of atopic conditions. We further discuss emerging therapeutic strategies designed to target the regulatory networks that support IgE plasma cell survival, with the goal of attenuating chronic IgE-mediated pathology.