Allergen-specific immunoglobulin E and immunoglobulin G B-cell receptors (Allergen-specific IgE/IgG BCR)

Allergen-specific IgE and IgG B-cell receptors (BCRs) are membrane-bound immunoglobulins (mIgE and mIgG) located on the surface of B lymphocytes that serve as the primary sensors for environmental antigens (PubMed: 24857411). These receptors are central to the pathogenesis of allergic diseases; when an allergen binds to a specific IgE-BCR, it triggers intracellular signaling pathways, such as the Bruton's tyrosine kinase (BTK) cascade, leading to B-cell differentiation into IgE-secreting plasma cells (UniProt: P01854). While IgE-BCRs drive the hypersensitivity response, IgG-BCRs (particularly IgG4) are often associated with immune tolerance and the production of antibodies that can neutralize allergens before they trigger mast cell degranulation (PubMed: 26921306). Therapeutic interventions targeting these receptors, such as the monoclonal antibody quilizumab, specifically aim to deplete the pool of mIgE-bearing B cells by targeting the M1-prime extracellular segment, thereby reducing the overall capacity for IgE production (PubMed: 25213061). Additionally, small molecule inhibitors of BCR signaling are being developed to modulate the activity of these cells in chronic allergic conditions like asthma and atopic dermatitis (PubMed: 30103374).

Other names

Membrane-bound IgE (mIgE)Membrane-bound IgG (mIgG)Allergen-specific B-cell receptorSurface immunoglobulin ESurface immunoglobulin GmIgE-BCRmIgG-BCR

Drugs targeting these receptors function by depleting B-cell populations that express membrane-bound IgE, blocking the binding of specific allergens to the receptor to prevent activation, or inhibiting downstream signaling enzymes like Bruton's tyrosine kinase (BTK) to halt the allergic cascade and subsequent IgE secretion.