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. Author manuscript; available in PMC: 2022 Jul 20.
Published in final edited form as: Cell Rep. 2022 Jun 28;39(13):111011. doi: 10.1016/j.celrep.2022.111011

Figure 1. Alox15 deletion in the β cell enhances expression of β cell genes and reduces expression of proinflammatory genes.

Figure 1.

(A and B) Wild-type (WT) and Alox15−/− islets were stimulated with IFN-γ, IL-1β, and TNF-α for 6 h. After stimulation, the islets were co-cultured with WT macrophages and WT naive T cells for 96 h.

(A) Experimental schematic.

(B) T cell activation was quantified by flow cytometry for CD4+IFN-γ+, CD4+IL-17+, and CD4+FoxP3+ T cells. N = 3–7 biological replicates.

(C–G) NOD-Alox15loxP/+ mice were crossed with NOD-Pdx1PB-CreER™ mice to generate NOD-Cre+ and NOD-Δβ mice. At 6 weeks of age, the mice were administered 3 daily intraperitoneal injections of 2.5 mg of tamoxifen.

(C) Experimental design.

(D–F) Quantitative RT-PCR from isolated islets at 8 weeks of age for the indicated genes.

(G) Quantitative RT-PCR from isolated islets at 12 weeks of age for indicated genes. N = 3–5 biological replicates.

Data are expressed as the mean ± SEM. *p < 0.05.