The opposite would be classic cases of HP as characterized by bird fanciers lung where exposure could be insidious and long term. Since the function of CD4 + T cells in summer-type HP and those in bird fanciers lung was not compared, there is a possibility that the function of CD4+ T cells may not be identical depending on the disease. Taken together, we concluded that these data suggested that highly elevated CD8+ T cells might have a protective effect on the development of pulmonary fibrosis or that relatively increased CD4 + T cells might play an important role in the pathogenesis of pulmonary fibrosis.
Although Semenzato et al reported several types of cytotoxic activities of lymphocytes from lungs of patients with HP that could be directly related to the acute injury of the lungs, the precise mechanisms of the development of lung fibrosis in HP remain unknown. Recently, Selman et al reported the effect of lung T lymphocytes on fibroblasts in idiopathic pulmonary fibrosis and HP They observed a substantial increase in collagen synthesis is triggered by lympho-ldnes from patients with idiopathic pulmonary fibrosis and HP with fibrosis, but not from those with HP without fibrosis. These differences between the two disorders may be derived from the differences of T cell populations that accumulate in the lung. They also reported a significant decrease in degradation of collagen in patients with HP who developed lung fibrosis in comparison with those who did not. We raised a possibility that in the fibrosis group of HP, the accumulated CD4+ T cells trigger collagen synthesis and/or inhibit collagenolysis, resulting in lung fibrosis that is indistinguishable from idiopathic pulmonary fibrosis.
Further studies are required to understand whether CD8 + cells in the local milieu prevent the development of fibrosis or CD4 + T cells support the development of fibrosis.