Abstract
Unlike peritoneal macrophages from normal rats, which stimulate T-lymphocyte blastogenic responses, alveolar macrophages are highly inhibitory. However, alveolar macrophages collected from lungs previously exposed to an inflammatory agent develop the capacity to cooperate with T cells in these responses. Recent reports in this journal indicate that underlying inflammation greatly enhances the susceptibility of the lung to sensitization by inhaled antigen. It is suggested that inflammatory-induced changes in the population of alveolar macrophages, which abolish the inhibitory activity of the latter on proliferation of T cells, are intimately involved in the increased susceptibility of the lung to the development of cellular hypersensitivity that accompanies inflammation.