Transgenic mice were created with the Lymphocytic choriomeningitis virus (LCMV) nucleoprotein(NP) under the control of the human insulin promoter (HIP). RT-PCR analysis indicates that transgenic mice express LCMV-nucleoprotein in the pancreas and thymus. Naive transgenic female mice exhibit slightly accelerated diabetes onset (95% diabetic by 35 weeks of age) when compared to wildtype controls (80% diabetic by 35 weeks of age), with no significant difference in overall diabetes incidence by 40 weeks of age. Immunohistochemistry of pancreas at one-week post LCMV infection shows an early infiltration of CD8 T cells in transgenic mice.  Within 2 weeks of infection with LCMV HIP-NP mice exhibit rapid onset of diabetes compared to 6-8 months in infected B6.RIP-NP (Stock No. 004826) mice. LCMV infected transgenic mice exhibit upregulation of CXCR3 and CXCR10. This model provides a novel autoantigen expressed in pancreatic islet cells.  LCMV infected transgenic mice provide an inducible system of early onset diabetes. This LCMV inducible strain may provide a model for early onset diabetes.

These NOD mice are hemizygous for the Lymphocytic choriomeningitis virus nucleoprotein under the control of human insulin promoter (HIP). This model provides a novel autoantigen expressed in pancreatic islet cells.  LCMV infected transgenic mice provide an inducible system of early onset diabetes.

Typically mice are recovered in 12-16 weeks. Contact Customer Service to place an order or for more information.

<a target="_blank" href="https://www.jax.org/jax-mice-and-services/customer-support" rel="noreferrer">Contact Customer Service</a> for more information.