We have investigated the ability of genetically athymic (nude) rats to develop an eosinophilia to stimuli which are known to cause an eosinophilia in normal rats. Nude rats developed eosinophilia following (a) the pulmonary embolization of bovine gammaglobulin (BCG)-coated latex particles, and (b) experimental infection with the nematode parasite Ascaris suum. Eosinophilia in nude rats was not dependent on the presence of specific homocytotropic antibodies, haemagglutinating antibodies or allergic bronchoconstriction. In the latex-BCG system, all normal litter-mates (rnu/+) demonstrated haemagglutinating antibodies and a percentage demonstrated IgE and IgG2a homocytotropic antibodies to BGG in conjunction with BGG-induced bronchoconstriction. Nude rats failed to display any of these phenomena yet developed lung eosinophilia with an identical time course to that seen in their normal litter-mates. Similar observations were made following infection with A. suum. IgE antibodies were only demonstrable in normal litter-mates, which also demonstrated significantly higher levels of haemagglutinating antibodies to the parasite compared to those seen in the nude rats. However, the time course and magnitude of eosinophilia following infection with Ascaris was similar in each group. In addition, nude rats developed a significantly higher peripheral blood eosinophilia compared with normal litter-mates following secondary infection with Ascaris. In view of the immunological studies demonstrating the thymus deficiency and T-cell deficiency of the nude rat, it can either be proposed that eosinophilia is not exclusively under T-cell control or that a sub-population of T cells capable of mediating an eosinophil response exists in these animals.