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Fig. 5 | Arthritis Research & Therapy

Fig. 5

From: Augmented PFKFB3-mediated glycolysis by interferon-γ promotes inflammatory M1 polarization through the JAK2/STAT1 pathway in local vascular inflammation in Takayasu arteritis

Fig. 5

Signaling pathway of interferon (IFN)-γ mediating M1 polarization. AE Change in PFKFB3, iNOS, CD206, and signaling pathway proteins during M1 macrophage polarization; FI 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); JM 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 < 0.0001

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