Autoimmune type 1 diabetes (T1D) is inhibited in NOD mice transgenically expressing all E3 genes under control of a rat insulin promoter (RIPE3/NOD, Stock No. <a href="http://jaxmice.jax.org/strain/004320.html">004320</a>).  For dissecting the protective mechanisms afforded by various E3 genes, they were subdivided into RIP-driven transgene constructs. Strong T1D protection mediated at the beta-cell level characterized DL704/NOD mice (Stock No. <a href="http://jaxmice.jax.org/strain/004227.html">004227</a>) lacking the E3 gp19K gene suppressing MHC class I expression but retaining the 10.4K, 14.5K, and 14.7K genes inhibiting Fas- or TNF-alpha-induced apoptosis and TNF-alpha-induced NF-kB activation. Much weaker protection characterized DL309/NOD mice expressing the gp19K but not the 10.4K, 14.5K, and 14.7K genes. While RIPE3/NOD splenocytes had an unexpected decrease in ability to adoptively transfer T1D, splenocytes from both the DL704 and DL309 stocks efficiently did so.

These DL309/NOD mice express a transgene containing only the E3 gp19K gene of the adenovirus early region 3 genes under control of the rat insulin II promoter (RIP). Autoimmune type 1 diabetes (T1D) is weakly inhibited in these mice.

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

Typically mice are recovered in 12-16 weeks. <a target="_blank" href="https://www.jax.org/jax-mice-and-services/customer-support" rel="noreferrer">Contact Customer Service</a> to place an order or for more information.