Immunoglobulin E autoantibody (IgE autoantibody)

Immunoglobulin E (IgE) autoantibodies are a specialized subset of the IgE class that recognize and bind to self-antigens (autoantigens), a phenomenon often referred to as autoallergy [15, 22]. These autoantibodies play a pivotal role in the pathogenesis of various autoimmune and inflammatory diseases by triggering type I hypersensitivity-like responses [16, 19]. When IgE autoantibodies bind to their respective autoantigens, the resulting immune complexes cross-link high-affinity IgE receptors (FcεRI) on the surface of mast cells and basophils, leading to the rapid release of inflammatory mediators such as histamine, proteases, and leukotrienes [7, 17]. This mechanism is a key driver in conditions like Chronic Spontaneous Urticaria (CSU), where IgE targets antigens such as thyroid peroxidase (TPO) or IL-24, and Bullous Pemphigoid (BP), where it targets hemidesmosomal proteins like BP180 [6, 9, 23]. Therapeutic strategies targeting these autoantibodies primarily involve monoclonal antibodies like omalizumab, which sequester free IgE in the circulation and downregulate the expression of IgE receptors on effector cells, thereby interrupting the autoimmune inflammatory cascade [1, 10, 21].

Other names

Self-reactive IgEAutoallergic IgEAnti-self IgEAutoreactive IgE

Neutralization of free IgE, prevention of IgE binding to FcεRI, downregulation of FcεRI expression on mast cells and basophils, acceleration of IgE dissociation from receptors, and inhibition of IgE production via CD23-mediated pathways [1, 2, 7, 10, 21].