The relationship between mast cell degranulation, anaphylaxis, and the production of homocytotropic antibodies was examined in ICR mice after trichinella infection. It was found that the active cutaneous response to trichinella antigen had a rapid onset (within 2 weeks) and the sensitivity increased over a 9-week period after infection. Two types of mast cell degranulation were observed: (i) moderate, with few extracellular, deep-blue-staining granules (May-Grunwald-Giemsa), and (ii) "explosive," with many extracellular reddish-staining, swollen granules, indicating an apparent breakdown of cell membrane. The moderate type was observed primarily during the first 4 weeks after infection, whereas the explosive type predominated during 5 to 8 weeks. Homocytotropic antibody of the immunoglubulin G(1) type appears responsible for moderate type degranulation, and mouse immunoglobulin E appears responsible for the explosive degranulation. No correlation was evident between the active cutaneous anaphylactic response and either type of degranulation or between active cutaneous anaphylaxis and circulating levels of homocytotropic antibody. A proposed role of immunoglobulin G(1) and mouse immunoglobulin E in immunity is discussed.