Immunologically mediated lung disease—introduction

The spectrum of pulmonary immune disease encompasses forms of acute, reversible, predominantly airway disease (e.g., acute asthma) and forms with chronic, irreversible, largely interstitial changes (e.g., pulmonary fibrosis). Significant overlap between these disease categories does occur, as evidenced by the induction of pulmonary fibrosis in certain subjects with allergic bronchopulmonary aspergillosis. This symposium updates information on both of these important clinical groupings--asthma and pulmonary fibrosis---and includes a discussion of occupational lung disease and pulmonary manifestations of the collagen vascular diseases. We begin with a discussion of delayed or late-phase responses in asthma and subsequently describe two disease syndromes, allergic bronchopulmonary aspergillosis and mold-sensitive asthma, which are associated with latephase pulmonary responses. Information in each of these reviews supports the concept that delayed-in-time asthmatic responses represent clinically important expressions of allergic respiratory disease. Polyclonal cell activators (silica, asbestos) and their role in pulmonary immune disease (e.g., silicosis) have recently received detailed investigative attention. Therefore, a discussion of this important topic is included here. Sarcoidosis and the pneumoconioses share a number of pulmonary architectural and immunologic changes. The importance of pulmonary T lymphocytes as regulators of disease activity in sarcoidosis and the significance of pulmonary macrophages as regulators of disease expression in silicosis are discussed in separate informative articles. In addition to the pneumoconioses, occupational lung disease induced by reactive chemicals represents a clinically important form of pulmonary immune disease. Accordingly, this topic is reviewed with special reference to disease induced by trimellitic anhydride. Finally, although an increased frequency of autoantibodies (antinuclear antibodies, rheumatoid factors) are commonly observed in several pulmonary immune diseases (e.g., sarcoidosis, silicosis, asbestosis), the pulmonary man-ifestations of the collagen vascular diseases reflect distinct disease forms and