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Background Chronic rhinosinusitis with nasal polyps (CRSwNP) is often characterized by local production of polyclonal IgE-idiotypes. Whilst tissue IgE concentrations can be in the range of several thousand kU/L, the regulatory mechanisms by which IgE-mediated inflammation is controlled in the nasal polyps is not well understood. Objective We sought to determine whether locally induced IgG antibodies in the nasal polyps can inhibit IgE-mediated pro-allergic response. Methods Nasal polyp homogenates were collected from grass pollen allergics with CRSwNP and non-allergic controls. IgE levels were measured by ISAC. IgE-containing nasal polyp homogenates, with/without IgG depletion, were evaluated for their capacity to promote IgE-facilitated allergen presentation, basophil activation and histamine release. Local IgE and IgG repertoires were evaluated by Immunoglobulin 454 sequencing. Results We show that IgG plays a key role in controlling IgE-mediated inflammatory responses in nasal polyps. Depletion of IgG from nasal homogenates resulted in an increase in CD23-mediated IgE-facilitated allergen binding to B cells (IgE-FAB), but also enhanced FcεRI-mediated allergen driven basophil activation and histamine release. A similar response was observed in relation to specific IgE antibodies to Staphylococcus aureus (SE-IgE). The capacity of IgG in nasal polyps to limit IgE-mediated inflammation is based on the fact that IgG repertoires widely share the antigen targets with the IgE repertoires, in both allergic and non-allergic subjects. Conclusion Polyclonal IgE idiotypes in CRSwNP are functional, promote IgE-mediated pro-allergic inflammation and are partially antagonized by corresponding IgG-idiotypes. This is most likely due to the fact that IgE and IgG clonotypes are widely shared in nasal polyps.