Abrogating IL-17 prior to infection in mice has been shown to improve outcome, suggesting hyperresponsiveness to infection in the airways of patients and consequent damage via neutrophils.48 Bullous pemphigoid (an immunobullous disease affecting the skin), shares target antigens to circulating autoantibodies in the BMZ, for example, BP180.1,49,50 Neutrophil elastase induces subepithelial blisters in a murine model of this disease, with elastase-deficient mice being resistant to subepithelial blistering.51 Neutrophil serine proteases may also play a role in fibrosis. The gene discussed is IL17A; the disease is infection.