The animal-model studies discussed above appear to suggest that AA develops as the result of a complex series of immunologically specific events, involving initial sensitization, and the development of granulomatous inflammatory response by a series of genetically determined immunostimulatory events. Modulation of experimental granulomatous lesions by several of the means previously discussed may offer some important clues to the incidence and clinical course of AA in man and to future therapy and/or prevention of the disease. For example, in the animal models discussed previously in which chronic exposure to aerosolized antigen resulted in specific 'desensitization' it is possible that such repeated challenge in man may be refined to the point of inducing similar lengthy refractory periods and a decrease in pulmonary inflammation. The demonstration that hypersensitivity-type pulmonary granulomas in mice are markedly suppressed by inhibitors possessing antilipoxygenase activity, such as nafazatrom and nordihydroguairetic acid and by cyclosporine, may also open the door to investigation of such agents in the experimental treatment of granulomatous pulmonary diseases in man. It is obvious that a better understanding of these mechanisms in man can provide important information to increase our understanding of the possible prevention, modulation, and therapy of chronic granulomatous pulmonary disease.