Persistent MHV (mouse hepatitis virus) infection reduces the incidence of diabetes mellitus in non-obese diabetic mice

Wilberz, S.; Partke, Hans-Joachim; Dagnæs‐Hansen, Frederik; Herberg, L.

doi:10.1007/bf00404016

Cited by 126 publications

(71 citation statements)

References 18 publications

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“…Single-cell suspensions were prepared and erythrocytes were lysed with NH 4 Cl as described elsewhere (25). Cells were washed twice with PBS and resuspended in high-glucose DMEM containing 10% heat-inactivated FBS, 1 mM sodium pyruvate, 100 U/ml penicillin, 0.1 mg/ml streptomycin, and 50 mM 2-ME (Life Technologies, Grand Island, NY).…”

Section: Cell Isolation Procedures and Flow Microfluorometrymentioning

confidence: 99%

“…Human studies of the interaction of environment and genetic predisposition are exceedingly difficult. The most widely used animal model of autoimmune diabetes, the nonobese diabetic (NOD) 4 mouse, models the process poorly because the overwhelming majority of perturbants reduce the frequency of diabetes and often prevent it entirely (2). Among murine viruses, encephalomyocarditis virus (3), mouse hepatitis virus (4), lymphocytic choriomeningitis virus (5), and others reduce the frequency of disease (6).…”

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confidence: 99%

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Infections That Induce Autoimmune Diabetes in BBDR Rats Modulate CD4+CD25+ T Cell Populations

Zipris

Hillebrands

Welsh

et al. 2003

The Journal of Immunology

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Viruses are believed to contribute to the pathogenesis of autoimmune type 1A diabetes in humans. This pathogenic process can be modeled in the BBDR rat, which develops pancreatic insulitis and type 1A-like diabetes after infection with Kilham’s rat virus (RV). The mechanism is unknown, but does not involve infection of the pancreatic islets. We first documented that RV infection of BBDR rats induces diabetes, whereas infection with its close homologue H-1 does not. Both viruses induced similar humoral and cellular immune responses in the host, but only RV also caused a decrease in splenic CD4+CD25+ T cells in both BBDR rats and normal WF rats. Surprisingly, RV infection increased CD4+CD25+ T cells in pancreatic lymph nodes of BBDR but not WF rats. This increase appeared to be due to the accumulation of nonproliferating CD4+CD25+ T cells. The results imply that the reduction in splenic CD4+CD25+ cells observed in RV-infected animals is virus specific, whereas the increase in pancreatic lymph node CD4+CD25+ cells is both virus and rat strain specific. The data suggest that RV but not H-1 infection alters T cell regulation in BBDR rats and permits the expression of autoimmune diabetes. More generally, the results suggest a mechanism that could link an underlying genetic predisposition to environmental perturbation and transform a “regulated predisposition” into autoimmune diabetes, namely, failure to maintain regulatory CD4+CD25+ T cell function.

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Section: Cell Isolation Procedures and Flow Microfluorometrymentioning

confidence: 99%

mentioning

confidence: 99%

Infections That Induce Autoimmune Diabetes in BBDR Rats Modulate CD4+CD25+ T Cell Populations

Zipris

Hillebrands

Welsh

et al. 2003

The Journal of Immunology

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“…This lack of ␤-cell autoimmune destruction could indicate either no triggering effect of cow's milk or an interference with protective effects possibly induced by frequent infections and the absence of a vaccination program in Yemen (14). The influence of infection has also been demonstrated in two animal models of type 1 diabetes-NOD mice and BB rats-in which differences in nutrition and housing conditions led to great differences in the incidence of diabetes (15)(16)(17).…”

Section: Correspondence Analysismentioning

confidence: 99%

Type 1 Diabetes Environmental Factors and Correspondence Analysis of HLA Class II Genes in the Yemenite Jewish Community in Israel

et al. 2001

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OBJECTIVE -The Israeli Yemenite Jewish community has displayed an exceptionally rapid increase in the frequency of type 1 diabetes, having the highest rate of all Israeli ethnic groups. We studied the role of the environment, in relation to the nature and frequency of HLA class II genes, to evaluate its possible involvement in the development of diabetes.RESEARCH DESIGN AND METHODS -We interviewed 196 elderly Yemenite women, who had immigrated to Israel as adults, in programmed encounters about signs and symptoms of type 1 diabetes, infant feeding customs, and infectious diseases in Yemen. We also performed HLA oligotyping of DRB1, DQA1, and DQB1 genes in 120 unrelated Yemenite Jews, including 44 type 1 diabetic patients and 76 healthy control subjects, and used these data in correspondence analysis comparing Yemenites with different Israeli ethnic groups.RESULTS -Interviews indicated that early exposure to cow's milk was very common in Yemen. However, none of the women could recall classical presentations of diabetes. HLA oligotyping showed that gene frequencies of non-Asp-57 (of the HLA-DQB chain) in the patients (0.94) and control subjects (0.6) were similar to those of other populations with a known high incidence of type 1 diabetes. Correspondence analysis revealed that Yemenite Jews are genetically distinct from other ethnic groups in Israel.CONCLUSIONS -The genetic distinctiveness of Yemenite Jews may explain their unusually high incidence of type 1 diabetes in Israel. Despite the presence of highly susceptible diabetogenic HLA class II genes in this community, early exposure to cow's milk did not cause phenotypic expression of diabetes in Yemen. This finding suggests that in this population, either cow's milk does not play a crucial role in triggering diabetes, or environmentally conferred protection, such as frequent infectious disease in Yemen, was dominant. Diabetes Care 24:650 -653, 2001

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“…For example, rates of Caesarean section in England, Sweden and the USA have risen from 6%, 8% and 10% in 1975 [5] to 19%, 12% and 22% in 1999 [4], respectively. Animal models suggest a higher risk of diabetes after Caesarean section [6,7]. Also, children delivered by Caesarean section have been shown to have altered gut microbiotic composition and immune function [8][9][10][11], which could increase their risk of type 1 diabetes.…”

Section: Introductionmentioning

confidence: 99%

Caesarean section is associated with an increased risk of childhood-onset type 1 diabetes mellitus: a meta-analysis of observational studies

et al. 2008

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Aims/hypothesis The aim of this study was to investigate the evidence of an increased risk of childhood-onset type 1 diabetes in children born by Caesarean section by systematically reviewing the published literature and performing a meta-analysis with adjustment for recognised confounders. Methods After MEDLINE, Web of Science and EMBASE searches, crude ORs and 95% CIs for type 1 diabetes in children born by Caesarean section were calculated from the data reported in each study. Authors were contacted to Diabetologia (2008) 51:726-735

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Persistent MHV (mouse hepatitis virus) infection reduces the incidence of diabetes mellitus in non-obese diabetic mice

Cited by 126 publications

References 18 publications

Infections That Induce Autoimmune Diabetes in BBDR Rats Modulate CD4+CD25+ T Cell Populations

Infections That Induce Autoimmune Diabetes in BBDR Rats Modulate CD4+CD25+ T Cell Populations

Type 1 Diabetes Environmental Factors and Correspondence Analysis of HLA Class II Genes in the Yemenite Jewish Community in Israel

Caesarean section is associated with an increased risk of childhood-onset type 1 diabetes mellitus: a meta-analysis of observational studies

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