Fig. 5From: Augmented PFKFB3-mediated glycolysis by interferon-γ promotes inflammatory M1 polarization through the JAK2/STAT1 pathway in local vascular inflammation in Takayasu arteritisSignaling pathway of interferon (IFN)-γ mediating M1 polarization. A–E Change in PFKFB3, iNOS, CD206, and signaling pathway proteins during M1 macrophage polarization; F–I expression of CD80, HLA-DR, CD163, and CD206 were detected by flow cytometry in M1 macrophage in the presence of a JAK inhibitor (tofacitinib, 10 nM) and a STAT1 inhibitor (fludarabine, 1 nM); J–M different cytokines (IL-1β, IL-6, IL-10, and TNF-α) were detected in M1 macrophage culture supernatant in the presence of a JAK inhibitor (tofacitinib, 10 nM) and a STAT1 inhibitor (fludarabine, 1 nM); n = 8. LPS (50 ng/ml) was added in all the groups besides the IFN-γ (20 ng/ml) or tofacitinib (10 nM) or fludarabine (1 nM) as indicated in the figures. Data revealed as mean ± SEM, *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001; ##p < 0.01; ###p < 0.001; ####p < 0.0001Back to article page