Nevertheless, these observations are of great interest to us from the point of view of a possible role for IgE-mediated mechanisms in asthma, since we have previously reported data suggesting that IgE is expressed to excess in the bronchial mucosa of asthmatic patients regardless of conventional atopic status,25, 26 and the additional presence of systemic IgG anti-IgE autoantibodies capable of directly activating cells bearing sufficient surface-bound IgE27 could represent a mechanism for local, allergen-independent disease exacerbation. Here, IGHE is linked to asthma.