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, nonsteroidal anti-inflammatory drugs-exacerbated respiratory disease, and
chronic spontaneous urticaria) to consider which
IgE-mediated mechanisms are relevant to nasal polyposis pathology. A type 2 eosinophil-dominated inflammatory signature is typical in
nasal polyp tissue of European patients with nasal polyposis, with a shift toward 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
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 on various cells, causing release of inflammatory mediators. The efficacy of
omalizumab confirms
IgE as an important inflammatory mediator in nasal polyposis. By blocking
IgE,
omalizumab targets the T2
inflammation in nasal polyposis, reduces
nasal polyp score and improves symptoms.