Anti-IgE for the treatment of allergic rhinitis - and eventually nasal polyps?

In allergic rhinitis, cross linking of IgE molecules upon allergen contact induces degranulation of mast cells and basophils within the mucosal tissue, and results in the release of typical mediators, which consecutively induce the well-known symptoms. Omalizumab counteracts these interactions by a reduction in serum levels of free IgE. Therapy targeted against IgE also interferes with its binding to the high- as well as the low-affinity receptors, inhibiting the amplification of the Th2-type response. Treatment of allergic rhinitis with anti-IgE has been shown to be safe and to reduce specific symptoms. Furthermore, the combination of omalizumab with specific immunotherapy (SIT) may offer not only an increase in efficacy, but also in safety in appropriate patients. The currently available studies with omalizumab in allergic rhinitis, as monotherapy or in combination with immunotherapy, are summarized. In nasal polyp disease, a local polyclonal IgE response has recently been described, initiated by Staphylococcus aureus-derived enterotoxins, which at least modifies the inflammatory reaction within the tissue. Evidence accumulates that these enterotoxins act as superantigens resulting in a polyclonal T- and B cell activation with massive IgE formation within the airways. Because of the polyclonality, a range of allergens could possibly maintain a constant degranulation of mast cells present in polyp tissue, which may contribute to the disease severity. We here discuss a proof-of-concept treatment trial with omalizumab in nasal polyposis, which in case of a positive therapeutic response, also would open the door for anti-IgE treatment approaches for severe nonatopic lower airway disease.