These include antinuclear antibodies in 34% of COPD patients at first exacerbation2, anti-elastin antibodies3 that correlate with emphysema severity, anti-epithelial cell antibodies4, IgG and C3 deposition in the small airways (indicative of antibody-mediated complement activation)48, neutrophil granule protein5, and a range of other autoantibodies6. This evidence concerns the gene C3 and chronic obstructive pulmonary disease.