The first report of hypersensitivity pneumonitis (HP) was in 1932 by Campbell as a disease caused by exposure to moldy hay in farmers. In 1959, Pepys first showed that acute (nonfibrotic) HP is an allergic disease. The first report of chronic (fibrotic) HP was published in 1968 by Seal, which included three cases transitioning to chronic disease. There are more than 300 inhaled antigens, including bacteria, fungi, animal-derived proteins, and low-molecular-weight compounds. In the pathogenesis of HP, inciting antigens react with specific antibodies (type III allergy) or sensitized lymphocytes (type IV allergy). In the chronic phase, this immune pathology changes as the immune response shifts from Th1 to Th2, depending on the type and amount of the causative antigen, and genetic factors.