Summary In summary, it appears that factors such as smoking and the presence of secondary Sjögren's syndrome might be important in predisposing the rheumatoid patient to the development of lung disease. Genetic factors may moderate or magnify these risks. At a cellular level, specific macrophage colonies within the lung may interact with a subgroup of CD4 T lymphocytes to produce unopposed B-cell activation, leading to local IgM production and the formation of immune complexes. This can damage lung both directly by cytolysis and indirectly by granulocyte recruitment through the release of neutrophil chemotaxins. Early in the evolution of these processes, steroids appear able to reduce lymphocyte numbers and prevent lung damage occurring, presumably by immunological mechanisms, while later they may reduce granulocyte numbers and activity, halting further progression of lung disease in some patients, perhaps by a direct anti-inflammatory effect. Confirmation of these mechanisms and the development of more specific therapeutic tools is probably dependent on studies which examine lung tissue directly by biopsy and may be aided by the application of more sensitive imaging techniques.