AntigenIgE

AntigenIgE refers to the interaction between an antigen, typically an allergen, and immunoglobulin E (IgE) antibodies that are bound to high-affinity FcεRI receptors on mast cells and basophils. In sensitized individuals, IgE antibodies produced against a specific antigen bind that antigen, and the IgE remains anchored on the cell surface. When the same antigen is encountered again, it can cross-link adjacent IgE-FcεRI complexes, initiating signaling that leads to cell activation.

Cross-linking triggers a cascade resulting in degranulation and the release of mediators such as histamine, leukotrienes, prostaglandins, and various cytokines. These mediators cause the acute symptoms of IgE-mediated hypersensitivity, including itching, swelling, rhinorrhea, urticaria, bronchoconstriction, and in severe cases anaphylaxis. The response is highly antigen-specific; it depends on class switching to IgE in B cells, driven by helper T cell cytokines (notably IL-4 and IL-13) and CD40-CD40L interactions.

Common sources of antigens include pollens, animal dander, dust mites, molds, and certain foods. IgE sensitization can be assessed by measuring total IgE levels or specific IgE to particular antigens, though sensitization does not always predict clinical allergy. Therapeutic approaches include anti-IgE antibodies (e.g., omalizumab) that reduce circulating IgE and FcεRI engagement, and allergen immunotherapy, which aims to modify the immune response and lower IgE over time.

In summary, antigenIgE describes the antigen-specific binding of IgE to FcεRI on effector cells and the cross-linking that triggers allergic inflammation in susceptible individuals.