In the pathogenesis of hypersensitivity pneumonitis (HP) several immune mechanisms are involved. The initial phase, 4-48 h after antigen inhalation, appears to be immune complex mediated and is characterized by an early increase in bronchoalveolar lavage (BAL) neutrophils and the histopathologic features of oedema, neutrophil infiltration of the alveolar wall, and vasculitis. After 12 h to several days, the immune response possibly shifts to a cell-mediated reaction, and the alveolitis consists of cytotoxic effector cells as well as suppressor cells which may be required to modulate the B cell response of antibody production by plasma cells. In this phase, lymphocytes of the OKT8 positive phenotype, natural killer cells, and occasionally a few plasma cells are increased in BAL fluid. The characteristic histopathologic finding is a mononuclear infiltrate consisting of lymphocytes, plasma cells, and foamy histiocytes. After weeks to months, a delayed type hypersensitivity reaction may lead to a slight predominance of OKT4 positive cells in BAL fluid and to granuloma formation. Finally, after months to years, repeated immune-mediated injury to the alveolar wall with release of proteolytic enzymes and fibroblast growth factors may result in pulmonary fibrosis and end stage lung with concomitant increase in BAL neutrophils as in other fibrotic diseases.