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="https://www.jax.org/strain/004320"">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="https://www.jax.org/strain/004227"">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.

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