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. Author manuscript; available in PMC: 2021 Apr 27.
Published in final edited form as: Sci Signal. 2020 Oct 27;13(655):eaay9217. doi: 10.1126/scisignal.aay9217

Fig. 7: PKM2 activator treatment redirects TH17 cells to adopt an encephalitogenic program.

Fig. 7:

(A) Schematic showing the stimulation of splenocytes from 2D2 mice and passive EAE induction. (B) Flow cytometry analysis of IL-17A and GM-CSF production by TCRβ+CD4+ cells on the day of splenocyte transfer. *p<0.05 by repeated measures one-way ANOVA with Tukey post test. (C) EAE phenotypes observed at day 16 post transfer of splenocytes treated with TEPP-46 (50μM) or vehicle (DMSO). Data shown are from n=19 DMSO- and n=24 TEPP-46-treated Rag1−/− mice that received 2D2 cells, pooled from four independent experiments. (D) Flow cytometry analysis of MHC-II and Ly6G expression on myeloid cells (defined as live, singlet, CD45hiCD11b+ cells) isolated from the indicated parts of the CNS of Rag1−/− mice receiving DMSO- or TEPP-46-treated cells. Data are expressed as mean ± SEM from n=10–12 mice per group pooled from N=2 independent experiments. Two-tailed Welch’s t-test. *p<0.05. (E) Representative images (left panels) of anti-CD45 staining in the periventricular brain regions from recipients of DMSO- or TEPP-46-treated splenocytes and quantification (right panel) or mice presenting with perivascular infiltrates. Data are compiled from two independent experiments with a total of 6 mice. Scale bar is 400 μm.