Allergen-specific IgE-producing B cell (IgE+ B cell)

Allergen-specific IgE-producing B cells are a specialized subset of B lymphocytes that have undergone class-switch recombination to express and secrete Immunoglobulin E (IgE) antibodies specific to environmental allergens (Wu and Zhai, 2011, PMID: 21844396). These cells play a central role in the pathogenesis of Type I hypersensitivity reactions, including allergic asthma, hay fever, and anaphylaxis, by serving as the source of IgE that sensitizes mast cells and basophils (Gould and Sutton, 2008, PMID: 18283160). Upon exposure to an allergen, these B cells can differentiate into plasma cells that secrete high levels of IgE, which then binds to high-affinity receptors (FcεRI) on effector cells. Therapeutic strategies targeting these cells aim to reduce the overall pool of IgE-producing cells or prevent their formation to lower serum IgE levels. For instance, Quilizumab was developed to target the M1' segment of membrane-bound IgE (mIgE) to deplete these specific B cells via apoptosis or ADCC (Gauvreau et al., 2014, PMID: 24746244). Other agents like Dupilumab indirectly target this population by blocking IL-4 and IL-13 signaling, which is essential for the initial class-switching of B cells to the IgE isotype (Gandhi et al., 2016, PMID: 26633315). By reducing the number of these B cells, clinicians hope to achieve long-term disease modification in allergic conditions by addressing the underlying source of pathogenic antibodies.

Other names

IgE-switched B cellsIgE-expressing B cellsIgE+ B lymphocytesAllergen-specific B cells

Depletion of membrane IgE-positive B cells via antibody-dependent cellular cytotoxicity (ADCC) and apoptosis (Gauvreau et al., 2014, PMID: 24746244); inhibition of B cell class-switch recombination to IgE by blocking IL-4/IL-13 signaling (Gandhi et al., 2016, PMID: 26633315); and neutralization of secreted IgE to prevent binding to high-affinity FcεRI receptors (Gould and Sutton, 2008, PMID: 18283160).