Allergen-specific B cells and plasma cells

Allergen-specific B cells and plasma cells are the primary cellular drivers of Type I hypersensitivity reactions and chronic allergic diseases. Upon initial exposure to an allergen, B cells undergo class-switch recombination to produce Immunoglobulin E (IgE), which subsequently sensitizes mast cells and basophils by binding to high-affinity FcεRI receptors. While memory B cells provide a long-lasting reservoir that can rapidly differentiate into IgE-secreting cells upon re-exposure, long-lived plasma cells residing in the bone marrow can maintain high serum IgE levels for years without further allergen contact. Targeting these specific cell populations represents a disease-modifying approach intended to eliminate the underlying 'allergic memory' rather than merely suppressing downstream symptoms. Current therapeutic interventions include monoclonal antibodies that deplete mIgE-positive B cells or block the cytokines required for IgE switching, such as IL-4 and IL-13. By reducing the population of these cells, clinicians aim to achieve long-term remission in patients with severe asthma, food allergies, and other atopic conditions.

Other names

IgE-producing B cellsIgE-secreting plasma cellsAllergen-specific memory B cellsmIgE-positive B cellsIgE-switched B cells

Therapeutic strategies targeting these cells involve the depletion of B cells expressing membrane-bound IgE (mIgE) through antibody-dependent cellular cytotoxicity (ADCC), the inhibition of IL-4 and IL-13 signaling to prevent B cell class-switch recombination to the IgE isotype, or the use of BTK inhibitors to disrupt B cell receptor signaling. Additionally, general B cell depletion via anti-CD20 therapies or targeting survival factors for long-lived plasma cells in the bone marrow aims to reduce the reservoir of allergen-specific antibody production.