Depressed immunological defence mechanisms in mice with experimentally induced diabetes.
Persistent diabetes mellitus with marked hyperglycemia was induced in mice by the administration of streptozotocin. In these streptozotocin-induced diabetic mice, resistance to tubercle bacillus challenge and primary as well as secondardy humoral immune responses against foreign erythrocytes were markedly depressed. The T-cell function in delayed hypersensitivity to 2,4-dinitro-1-fluorobenzene and bacterial phagocytic activity or peritoneal macrophages were markedly depressed. In contrast, the B-cell function in antibody production against T-independent antigen and the intracellular killing of bacteria in peritoneal macrophages were intact. We concluded that depression of the T-cell function or the phagocytic activity of macrophages or both may be the main immunological defect in these mice.
D000818:Animals; D000917:Antibody Formation; D001402:B-Lymphocytes / Q000276:immunology; D003921:Diabetes Mellitus, Experimental / Q000276:immunology*; D004912:Erythrocytes / Q000276:immunology; D005951:Glucose Tolerance Test; D006968:Hypersensitivity, Delayed; D007156:Immunologic Memory; D008264:Macrophages / Q000276:immunology; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D010587:Phagocytosis; D013601:T-Lymphocytes / Q000276:immunology*; D014376:Tuberculosis / Q000276:immunology