Altered immune reactivity in encephalomyocarditis-M variant (EMC-M)-induced diabetes in mice.
Approximately 50% of DBA/2j male mice infected with EMC-M develop glycosuria with suppressed immune responsiveness to the mitogens PHA, Con A and PWM. The greatest degree of suppression was noted with Con A treated cultures. In vivo treatment with Levamisole, a known T cell stimulant, especially increased the response to Con A but exacerbated the diabetogenic state as reflected by increased occurrence of glycosuria. Virus infected mice, given anti-lymphocyte serum (ALS), showed marked amelioration of the diabetic syndrome. Indomethacin, a non-steroidal anti-inflammatory agent as well as a prostaglandin-synthetase inhibitor, partially reversed the in vitro splenic cell suppression of infected animals.
D000818:Animals; D000961:Antilymphocyte Serum / Q000494:pharmacology; D003208:Concanavalin A / Q000494:pharmacology; D003921:Diabetes Mellitus, Experimental / Q000276:immunology*; D004686:Encephalomyocarditis virus; D004769:Enterovirus Infections / Q000209:etiology / Q000276:immunology*; D014644:Genetic Variation; D006029:Glycosuria / Q000209:etiology; D007165:Immunosuppression Therapy; D007213:Indomethacin / Q000494:pharmacology; D007978:Levamisole / Q000494:pharmacology; D008297:Male; D051379:Mice; D008811:Mice, Inbred DBA; D010835:Phytohemagglutinins / Q000494:pharmacology; D011043:Pokeweed Mitogens / Q000494:pharmacology
D000961:Antilymphocyte Serum; D010835:Phytohemagglutinins; D011043:Pokeweed Mitogens; D003208:Concanavalin A; D007978:Levamisole; D007213:Indomethacin