By Hans-Georg Joost, Hadi Al-Hasani, Annette Schürmann

Detailing the newest protocols for studying animal versions of diabetes, in particular resistant teams of rodents resembling the NOD mouse, and together with specialist suggestion on implementation, this can be a beneficial new quantity within the tools in Molecular Biology sequence.

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Endocrinology 136:5731–5735 9. Shin JH, Janer M, McNeney B et al (2007) IA-2 autoantibodies in incident type I diabetes patients are associated with a polyadenylation signal polymorphism in GIMAP5. Genes Immun 8:503–512 10. Hellquist A, Zucchelli M, Kivinen K et al (2007) The human GIMAP5 gene has a common polyadenylation polymorphism increasing risk to systemic lupus erythematosus. J Med Genet 44:314–321 11. Hornum L, Romer J, Markholst H (2002) The diabetes-prone BB rat carries a frameshift 12.

Clinical data reveal that diabetes onset is often preceded by exposure to viral infections including mumps, rubella, rotavirus, parvovirus, and enteroviruses (57). In a recent metaanalysis of 26 cohort or case–control studies in which enterovirus RNA or viral protein was measured in blood, stool, or tissue of patients with pre-diabetes and diabetes, the authors reported a clinically significant association between enterovirus infection and T1D (58). This association between enterovirus infection and 3 BB Rat Model of Diabetes 35 diabetes was strong, with children at diagnosis of T1D ~10 times more likely to have an enterovirus infection than the diabetes-free control group.

Diabetes in BBDP rats can be prevented by blockade of costimulatory CD28 pathways, while blockade of the CD40-CD154 pathway has less effect (46). BBDP rats exhibit a severe imbalance between Th17 and regulatory T cells within the first months of age (47). Adoptive transfer of Treg cells, or in vivo expansion of Treg cells by treatment with a CD28 agonistic antibody, interferes with the development of diabetes in these animals, whereas treatment with conventional T helper (Th) cells does not afford protection.

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