By Hans-Georg Joost, Hadi Al-Hasani, Annette Schürmann
Detailing the most recent protocols for learning animal types of diabetes, specially resistant teams of rodents comparable to the NOD mouse, and together with specialist recommendation on implementation, it is a worthy new quantity within the equipment in Molecular Biology sequence.
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Ebook via Vatikiotis, P. J.
Detailing the most recent protocols for studying animal versions of diabetes, in particular resistant teams of rodents resembling the NOD mouse, and together with professional suggestion on implementation, this can be a worthwhile new quantity within the tools in Molecular Biology sequence.
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3. Prevention and Reversal of Diabetes in the Diabetes-Prone Rat Model The BBDP rat model has historically been used in many studies to discover and evaluate potential treatments to prevent or reverse autoimmune human T1D. Administration of parenteral insulin and certain dietary modifications can prevent or delay diabetes onset in the BBDP rat (34, 35). Insulin gene therapy has been tested in BBDP rats using adenovirus to deliver a glucose-regulated insulin transgene (36). Diabetes in BBDP rats can also be prevented by intrathymic islets transplantation (37).
However, these TLR ligands are unable to induce diabetes when used alone. The most potent protocol to induce T1D in the BBDR rat is the combination of KRV infection and low dosage of poly I:C treatment. This method induces nearly 100% diabetes within a time frame of 14–21 days after treatment. In the absence of KRV infection, poly I:C treatment at this dosage level is unable to induce diabetes (76, 77). Poly I:C, as a TLR3 agonist and viral mimetic, is well known for its ability to induce activation of the innate immune system.
Recent genetic studies suggest that a key diabetes 40 R. Bortell and C. Yang susceptibility locus in the BB and other diabetes-susceptible rat strains is an allele of the TCR Vbeta chain (97), raising the possibility that specific TCR alleles in humans may one day be associated with disease susceptibility. Together, such studies may identify potential new therapies for intervention to prevent T1D, especially those which allow select targeting of limited TCRs rather than broad, “across-the-board” suppression of all TCR signaling.