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. Author manuscript; available in PMC: 2024 Feb 1.
Published in final edited form as: Neuron. 2022 Sep 28;110(23):3936–3951.e10. doi: 10.1016/j.neuron.2022.09.002

Figure 7. Myeloid cell secretome-induced resistance reflects IFNβ content and can be reversed by JAK/STAT inhibition.

Figure 7

(A) ZIKV RT-qPCR of GBM E22 cultures 48 h.p.i. treated with exogenous recombinant IFNβ as indicated.

(B) STAT1 phosphorylation in GBM E22 cells harvested 3 hours post treatment with: (Upper) Recombinant IFNβ; (Middle) IFNβ +/-JAK1/2 inhibitor ruxolitinib; (Lower) 11b+CM and Pi:c-11b+CM +/-ruxolitinib (Rux).

(C) Normalised expression by qRT-PCR for the interferon stimulated genes indicated in GBM E22 and HDB FB1 cultures, in response to exogenous IFNβ at the indicated media concentrations, normalised to GAPDH expression and with gene expression in untreated HDB FB1 cells assigned the value 1.0.

(D) ZIKV RT-qPCR in HDB FB1 (left) and GBM E22 glioma stem cells (right) 48 h.p.i. or 48 hours with or without 24 hours pre-treatment with IFNβ (100 pg/ml) or Pi:c-11b+CM, +/-ruxolitinib 1000 nM. (unpaired t-test *p < 0.05, **p<0.01, ***p<0.001)

(E) HDB slice cultures harvested at 72 h.p.i., infected with ZIKV +/-IFNβ. Graph shows the percentage of SOX2+ cells infected with ZIKV versus total SOX2+ cells for the conditions indicated, MOCK is uninfected. n = total cells analysed across 3 slices per condition, 1-3 replicate cryosections per slice, in 1 HDB sample.