Abstract
Summer-type hypersensitivity pneumonitis (SHP) is the most prevalent type of HP in Japan, and the major causative agent of the disease is T. cutaneum. The major antigenic substance of the yeast is serotype-related polysaccharide. Home environmental factors indicate that SHP is a sick house syndrome. Immunologically, both humoral and cellular hypersensitivities are involved in the induction of the disease. The levels of specific IgG and IgA antibodies and complements in BAL fluids from SHP patients are well correlated to the clinical course. On the other hand, BAL lymphocytes in SHP patients are mostly T lymphocytes, mainly due to an increase in CD8+ subpopulations of lymphocytes; this leads to a decrease in the ratio of CD4+ to CD8+. These T cells belong to CD45RO+ memory T lymphocytes and LFA-11 alpha high+ cytotoxic T lymphocytes as assessed by their cell surface phenotypes. However, functions of these BAL T lymphocytes remain undefined. Host factors such as HLA-DQw3 and cigarette smoking may participate in the development of the disease. In conclusion, the pathogenesis of SHP is considered to be a combination of immune complex disease and cellular hypersensitivity to T. cutaneum.
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