Fig. 5: FFA2 βKO islets and mice show reduced T1-IFNs signaling.

Islets from floxed control or FFA2 βKO received either no treatment or 20,000 U/mL IFNα treatment for 2 h. The expression of T1-IFN-regulated genes (A), Ifit1, Ifit3, Ifit3b, and Oasl2, and negative regulators of T1-IFN signaling (B), Socs1 and Socs3, are shown in fold change relative to floxed control with matched IFNα treatment. Anti-IFNAR1 antibody was given to floxed control, Cre control, and FFA2 βKO male mice at a dose of 1 mg per mouse on days 0 and 6. Floxed and FFA2 βKO male mice treated similarly with IgG1 isotype served as controls. Both groups were given MLDS treatment to induce T1D. The random blood glucose level on the 7th day after the initial STZ injection (C) and diabetes incidence after the 21st day (D) in all groups are shown. The red dotted line in (D) indicates the 7th day, denoting the diabetes incidence difference between the IgG-injected floxed control and the IFNAR1 antibody-injected cre and floxed control. For (A), no treatment: N = 6 (floxed control) and 4 (FFA2 βKO); IFN α treatment: N = 4 for both. For (B), no treatment: N = 4 (floxed control) and 3 (FFA2 βKO); IFN α treatment: N = 5 (floxed control) and 4 (FFA2 βKO). For (C) and (D), N values are 6, 5, 6, 10, and 8 for IgG-injected floxed control, IgG-injected FFA2 βKO, IFNAR1 antibody-injected cre control, floxed control, and FFA2 βKO, respectively. Data are expressed as mean ± standard error and analyzed by Student’s t-test (A and B), one-way ANOVA with Holm-Šídák’s multiple comparisons (C), and Log-rank (Mantel–Cox) test (D). *p < 0.05, **p < 0.01, and ***p < 0.001. In (C) and (D), statistical significance was calculated compared to the floxed control + IgG group. For genotype and condition, blue bar and line = floxed control, green bar and line = FFA2 βKO, gray bar and line = Cre control. For antibody treatment, solid bar and line = IgG-injected groups, and dotted bar and line = IFNAR1 antibody-injected groups.