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. Author manuscript; available in PMC: 2021 Apr 28.
Published in final edited form as: Diabetes Obes Metab. 2020 Jul 5;22(10):1827–1836. doi: 10.1111/dom.14104

FIGURE 3.

FIGURE 3

TYK2 inhibition prevents IFNα-induced STAT1/2 phosphorylation and HLA-ABC, CXCL10, MX1 and CHOP upregulation in human islet cells. Dispersed human islets were left untreated (CTL) or pretreated with 1 μM of TYK2 inhibitor (iA and iB for TYK2iA and B, respectively) for 2 hours. Then IFNα (2000 U/mL) was added for 24 hours in the continuous presence of the inhibitors. (A) Protein expression was measured by western blot and representative images of six independent experiments are shown. Densitometry results are shown for pSTAT1 (B) and pSTAT2 (C) and the values were normalized by β-actin. The mRNA expression of HLA-ABC (D), CXCL10 (E), MX1 (F) and CHOP (G) was analysed by RT-qPCR and the values were normalized by β-actin. (H) CXCL10 protein secretion in the supernatant fraction was determined by ELISA. In all experiments, the values were normalized by cells treated with IFNα without TYK2 inhibitors, considered as 1. Results are mean ± SEM of six (A-G) or five (H) independent experiments. *P < .05, **P < .01 and ***P < .001 vs. control (CTL NT); †P < .05, ††P < .01 and †††P < .001 vs. CTL IFNα; one-way ANOVA. (I) ICC of MHC class I (red), insulin (green) and Hoechst (blue) in human islets treated with IFNα with or without TYK2 inhibitors as described above (magnification ×40)