Modern studies undertaken to aid the understanding of the pathogenesis of pulmonary sarcoidosis have shown that the initial lesions of this disease are characterised by an accumulation of T lymphocytes and of macrophages in the alveolar structure (the alveolitis). In patients with active disease these cells are seen to be not only increased but apparently "activated". In effect, in sarcoidosis the greater part of the T lymphocytes of the lung express surface markers associated with helper/inducer phenotype and they spontaneously secrete mediators which seem to play a central role in the formation of the typical lesions of this disease: a lymphocytic alveolitis, granulomas and interstitial fibrosis. As with the T lymphocytes, the alveolar macrophages of patients suffering from active sarcoidosis appear to be activated and are important in the initiation and maintenance of the inflammatory phenomena which lead to a modification of alveolar structures which are typical of this disease. However, although the immune and inflammatory cells situated in the lung modulate the lesions in the respiratory tree, it may be reasonable to propose the hypothesis that the evaluation of the clinical state of patients with sarcoidosis might take into account the degree of the alveolitis. The parameters of this alveolitis, which may help to establish the prognosis and need for therapy in pulmonary sarcoidosis, have not yet been discovered.