Figure 3

Protection from diabetes after myeloid-specific deletion of Alox15 in NOD mice. NOD mice harboring the Lyz2-Cre allele were crossed to NOD mice harboring Cre recombinase sites (Loxp) flanking exons 2–5 of the Alox15 gene to generate NOD:Alox15Δmyel mice (Δmyel). NOD:Lyz2-Cre (Cre+) and NOD:Alox15Loxp/Loxp littermates were used as controls. (A) Alox15 mRNA expression in peritoneal cells, spleen, and isolated islets (n = 3–4 per tissue); *P < 0.05 by unpaired 2-tailed t test. (B) Diabetes incidence in female mice. Number of mice per group is indicated. P value indicates significance by log rank test. (C) Diabetes incidence in male mice. Number of mice per group is indicated. P value indicates significance by log rank test. (D) Representative IHC images of mouse pancreata from Cre+ and Δmyel mice immunostained for insulin (brown) and counterstained with hematoxylin (blue). Scale bar: 1000 μm. (E) β Cell mass in Cre+ and Δmyel mice (n = 3–4 mice per genotype). (F) Insulitis scoring from pancreata of Cre+ and Δmyel mice (n = 3 mice per genotype). (G) Gene expression in isolated islets from Cre+ and Δmyel mice (n = 3 mice per genotype). For E–G, *P < 0.05 by unpaired 2-tailed t test. All data are presented as mean ± SEM.