Pulmonary fibrosis is commonly characterized by inflammation of the alveolar wall, leading to derangement of normal alveolar architecture, and interstitial as well as intra-alveolar fibrosis. The process involves cellular interactions via a complex cytokine network and heightened collagen gene expression with abnormal deposition in the lung. Recent studies have identified a myriad of cytokines with potential roles in pulmonary fibrosis. Based on in vivo antibody neutralization studies, important roles for tumor necrosis á (TNFá), macrophage inflammatory protein 1á (MIP-1á) and transforming growth factor (TGF), have been established. The recent demonstration that the eosinophil is a major source for several of these key pro-fibrogenic cytokines during the early stages of fibrosis, strongly suggest a role for the eosinophil in pulmonary fibrosis. In vitro, eosinophils can elaborate factors capable of stimulating fibroblast proliferation, and their presence in lungs undergoing many forms of pulmonary fibrosis has been well documented. Further support for a role for eosinophils in pulmonary fibrosis are suggested by clinical data showing a correlation between lung eosinophil count and a poor prognosis and decreased responsiveness to therapy. This review will focus on the recent findings, which suggest novel potential roles for the eosinophil in the pathogenesis of pulmonary fibrosis.