Functional subsets of human T cells defined by "active" rosette formation

Experiments were conducted defining the possible basis for increased susceptibility of alloxan-treated and genetically diabetic C57Bl/KsJ mice to infections with Candida albicans. Alloxan monohydrate (175 mg/kg) produced a prolonged state of hyperglycemia, which persisted through 31 days. Parameters of immune responses varied depending upon the interval between alloxan administration and testing. In the period immediately following alloxan treatment (1–14 days), the numbers of lymphocytes in the thymus and spleen were reduced, the numbers of recoverable peritoneal macrophages were decreased, and the mice showed an increased susceptibility to intravenous infection with C. albicans. In contrast, splenic lymphocytes responded normally to stimulation with Con A, and in vitro phagocytosis of yeast cells by peritoneal macrophages was normal. Also, in vivo production of such lymphokines as migration inhibitory factor (MIF) and macrophage activating factor (MAF), as well as delayed hypersensitivity footpad responses, was generally within the normal range. In the later phase of alloxan diabetes (21–28 days) after administration of alloxan, lymphoid cellularity recovered progressively and the numbers of recoverable peritoneal macrophages were normal. However, these mice still showed an increased susceptibility to C. albicans infection. Genetically diabetic mice (C57Bl/KsJ, db/db) were abnormal in virtually all the assays involving cell-mediated immunity. The numbers of lymphocytes and peritoneal macrophages were markedly decreased, lymphoid cells responded poorly to Con A, and the phagocytosis of yeast cells by macrophages was depressed. The in vivo production of lymphokines and footpad responses of the delayed-type hypersensitivity were depressed. In addition, these mice were highly susceptible to intravenous infection with C. albicans.