Beschreibung:
<jats:title>Abstract</jats:title>
<jats:p>Notoriously known for its involvement in type I hypersensitivities, Antigen (Ag)-specific IgE mediates a variety of mild to severe responses, including asthma. Ag-specific IgE is additionally important for immunity against gastrointestinal helminths, but these helminths also elicit production of low-affinity, poly-specific IgE. Helminth infection has been shown by several groups to be protective against asthma. The mechanisms behind these findings have included the induction of regulatory pathways, but the role of poly-specific or “benign” IgE has not been fully assessed. To test this in the absence of helminth infection, we utilized a four week model of murine asthma and injected IgE anti-DNP as our “benign” IgE twice a week. We found that treatment significantly reverses the eosinophil accumulation, airway hyperresponsiveness, and lung pathology seen with this model. Further analysis shows that the “benign” IgE treatment is only needed during the antigen challenge phase and not during sensitization phase. Using in vitro assays we were able to show that non-specific IgE can block Ag-specific IgE degranulation even after Ag-specific IgE pre-incubation. Overall, these data demonstrate a novel avenue for blockage of mast cell degranulation and a potential regulatory role for IgE.</jats:p>