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. Author manuscript; available in PMC: 2019 May 16.
Published in final edited form as: Nature. 2018 May 16;557(7707):724–728. doi: 10.1038/s41586-018-0119-x

Figure 3. Trp metabolites control microglia/astrocyte interactions and CNS inflammation.

Figure 3.

(a) Clinical scores in control and CX3CR1-AHR mice treated with TDD, TDD+Trp or TDD+I3S from day 21 after EAE induction (n=10 mice per group). Data are mean ± s.e.m. representative of two independent experiments. P values were derived by two-way ANOVA. n.s. not significant. (b) Microglia were isolated and subjected to RNA-sequencing. Heatmap of expressed genes of normalized reads of n = 2 independent samples per group. (c) t-distributed stochastic neighbor embedding (tSNE) plot of RNA-Sequencing data isolated from microglia of mice as in (b). (d) microglial mRNA expression determined by qPCR in EAE mice as in (a). Data are mean + s.e.m. representative of two independent experiments with n = 3 replicates. P values determined by one-way ANOVA followed by Tukey’s post-hoc test. (e) mRNA expression determined by qPCR in microglia from EAE mice as in (a). Data are mean + s.e.m. and representative of two independent experiments with n = 3 replicates. P values determined by one-way ANOVA followed by Tukey’s post-hoc test. (f) Heatmap depicting mRNA expression in astrocytes from EAE mice as in (a), as determined by RNA-seq of normalized reads of n = 2 independent samples per group.