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. 2020 Jun 13;69(8):1749–1762. doi: 10.2337/db19-0979

Figure 3.

Figure 3

Diabetes is delayed in RIP-RAE1ε NOD mice through interaction with NKG2D. A: Schematic of part of the vector used to generate the PCCALL-RAE1ε mice and breeding schema for generating NOD mice with constitutive RAE1ε expression in the islets. B and C: Diabetes development in female RIP-RAE1ε (n = 39) and control (PCCALL) (n = 21) and male RIP-RAE1ε (n = 23) and control (PCCALL) (n = 19) NOD mice. D: Diabetes development in female RIP-RAE1ε NKG2D-deficient (Klrk1−/−) (n = 11) and control (PCCALL/NKG2D-deficient [Klrk1−/−]) (n = 20) NOD mice. *P < 0.05, **P < 0.0008 by log-rank test. E and F: Insulitis scores in the pancreata of 9-week-old and 12-week-old RIP-RAE1ε and control (RIP-cre and PCCALL) mice. *P < 0.05 by Mann-Whitney U test.