What is the contribution of IgE to nasal polyposis?

Abstract

Taking a novel approach, this narrative review collates knowledge about nasal polyposis and the biological functions of IgE in several diseases (allergic rhinitis, allergic asthma, non-steroidal anti-inflammatory drugs-exacerbated respiratory disease [N-ERD] and chronic spontaneous urticaria) to consider which IgE-mediated mechanisms are relevant to nasal polyposis pathology. A type 2 (T2) eosinophil-dominated inflammatory signature is typical in nasal polyp tissue of European patients with nasal polyposis, with a shift towards this endotype observed in Asian populations in recent years. Elevated polyclonal IgE is present in the nasal tissue of patients with and without allergy. It is derived from many different B cell clones and, importantly, is functional (proinflammatory). Staphylococcus aureus (SA) enterotoxins are thought to act as superantigens, inducing production of polyclonal IgE via B-cell and T-cell activation, and triggering release of inflammatory mediators. In some patients, exposure to antigens/triggers leads to production of high levels of antigen-specific IgE which mediates cross-linking of the high-affinity IgE receptor (FcεRI) on a variety of cells, causing release of inflammatory mediators. The efficacy of omalizumab confirms IgE as an important inflammatory mediator in nasal polyposis. By targeting all free IgE, omalizumab can reduce nasal polyp size, improve symptoms and inhibit underlying T2 inflammation.