Chronic, acute and subacute inflammation within the lung as a result of bacterial, fungal, viral infection or of unknown etiologies constitutes one of the most frequent health problems within the United States. It is currently believed that T cells, B cells and macrophages interact with these foreign substances to eliminate them with the resultant induction of a cell mediated and/or humoral response that under normal circumstances protects the host against further damage by that agent or substance. The specific roles and mechanisms of these interactions are complex and not completely understood. Further, they do not always work for the benefit of the host and they may not effectively eliminate the infectious agent from the host. We have selected several mouse model systems that should permit us to dissect and reconstitute the functions of T cells, B cells and macrophages during host responses to several different organisms capable of inducing chronic pulmonary disease. Also, by combining the test organisms (Nocardia asteroides, Mycobacterium intracellulare, Candida) with our animal models we should be able to determine whether or not a dichotomy exists in T cell and B cell function in acute and chronic phases of infection. These studies should enable us to determine the specific ways these organisms alter or affect host responsiveness thay may permit them to overcome the defenses within the "normal" host.