Abstract
Asthma and allergic alveolitis are common clinical consequences of exposure to aerosolised antigens, although little is known about the factors that determine which outcome predominates. The isotype of the antibody response is one important determinant; IgE is associated with atopic asthma and IgG is associated with allergic alveolitis. The antibody isotype specificity to the same antigen in occupational settings can be determined by cigarette smoking. In a study of allergic lung disease in seafood processors, smokers produce IgE antibody levels and non-smokers produce IgG antibody to the same aerosolised antigen (p<0.001 for each). The specific IgE correlated with total IgE and the specific IgG correlated with the total IgG levels (p<0.01 for each) suggesting a major dichotomy of the humoral immune responses. Despite this, there is evidence that suggests common cellular control at the lymphocyte level. Asthma is IL-4 dependent and is associated with reduced CMI responses to tuberculin. In pigeon fanciers’ allergic alveolitis, there is no evidence of IgE antibody, but the in-vitro lymphocyte proliferative response to avian antigen is entirely IL-4 dependent (p<0.001) and the IgG response to avian antigen is associated with anergy to PPD (p<0.001). Allergic alveolitis is a prototype lymphocytic granulomatous disease and asthma is a prototype eosinophilic disease. Comparing the pathogenesis of these, occasionally associated with the same antigen exposure, may be a novel approach to broaden our understanding of both.