concanavalin-a and Enterovirus-Infections

The basis for the resistance of the female and the susceptibility of the male ICR Swiss mouse to the diabetogenicity of the D variant of encephalomyocarditis virus (EMCV-D) is unknown. This pattern of disease resistance and susceptibility can be reversed if females are treated with testosterone and males are treated with estrogen before virus infection. As a possible explanation for this sex difference in disease development, differences in early antiviral host responses were explored. Cellular antiviral resistance mechanisms operative early in virus infection were evaluated in ICR Swiss mice of both sexes after intraperitoneal infection with virus. No differences were seen in splenic natural killer (NK) cell responses of male and female mice during the 1st wk of infection, during which only the males became diabetic. Depletion of NK cell activity with rabbit anti-asialo GM1 serum did not render the infected ICR Swiss female susceptible to virus-induced diabetes. Treatment of ICR Swiss mice with type I carrageenan to compromise macrophage function rendered the female susceptible to diabetes after infection with EMCV-D but made only the male susceptible to diabetes by the usually avirulent interferon-inducing EMCV-D. Concanavalin A and recombinant interleukin 2, inducers of immune interferon, which in turn primes macrophages for activation and induces their expression of la antigens, protected the ICR Swiss male against the diabetogenic effects of EMCV-D. Interleukin 2 enhanced the male's capacity to exhibit an increase in the expression of Ia antigen by peritoneal exudate cells 1 day after injection with EMCU-D to a level seen in disease-resistant females.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Blood Glucose; Cell Line; Concanavalin A; Cytotoxicity, Immunologic; Diabetes Mellitus, Experimental; Encephalomyocarditis virus; Enterovirus Infections; Female; Interleukin-2; Killer Cells, Natural; Male; Mice; Mice, Inbred ICR

Immunogenetic mechanism may be involved in the pathogenesis of idiopathic cardiomyopathy. Viral myocarditis is considered a cause of dilated cardiomyopathy. In this study, we examined the major histocompatibility complexes (human leukocyte antigens: HLA) by microdroplet cytotoxicity test, lymphocyte subsets by laser flow cytometry, and the activity of lymphocyte blastoformation induced by phytohemagglutinin (PHA) and concanavalin A (Con A) in patients with cardiomyopathies (DCM) and myocarditis (MC). We also examined the incidence and histopathology of encephalomyocarditis (EMC) virus myocarditis in inbred strains of mice, and serial changes of T- and B-lymphocytes in the peripheral blood of DBA/2 mice inoculated with EMC virus by immunofluorescence techniques. The results were as follows: Major histocompatibility complex (HLA and H-2); HLA-B12 in patients with DCM and HLA-DR8 in patients with MC were more frequent than in controls. In EMC virus infection, differences were found in the frequency of occurrence of MC in inbred strains of A/J (H-2a), C57BL/6 (H-2b), BALB/c (H-2d), DBA/2 (H-2d) and C3H/He (H-2k) mice. Genetic mechanism may play a role heart similar to lesions in patients with DCM were seen in DBA/2 mice in the chronic stage of MC. in susceptibility to virus infection. Lymphocyte population study; OKT 8 (suppressor T-cell) was significantly lower in patients with DCM and hypertrophic cardiomyopathy (HCM) than in controls. There were no significant changes of lymphocyte subsets in patients with MC as compared with the controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Cardiomyopathy, Dilated; Concanavalin A; Encephalomyocarditis virus; Enterovirus Infections; HLA Antigens; Humans; Lymphocyte Activation; Lymphocytes; Major Histocompatibility Complex; Mice; Myocarditis; Phytohemagglutinins; T-Lymphocytes

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.

Topics: Animals; Antilymphocyte Serum; Concanavalin A; Diabetes Mellitus, Experimental; Encephalomyocarditis virus; Enterovirus Infections; Genetic Variation; Glycosuria; Immunosuppression Therapy; Indomethacin; Levamisole; Male; Mice; Mice, Inbred DBA; Phytohemagglutinins; Pokeweed Mitogens