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. 2019 Jul 16;8:e47117. doi: 10.7554/eLife.47117

Figure 7. Microglial-specific TLR4 signaling protects from neurologic disease.

(A) WT, TLR4-/-, WT mice receiving WT bone marrow and WT mice receiving TLR4-/- bone marrow were infected with JHMV and clinical scores (left) and area under curve (right) calculated. (B) Nestin-Cre or TLR4-fl/fl (as WT controls) (n = 12) and nestin-Cre TLR4-fl/fl (n = 5) were infected with JHMV and clinical scores (left) and area under curve (right) determined. Results representative of two independent experiments (C) TLR4 fl/fl (n = 6) (as WT controls) and CX3CR1CreER TLR4 fl/fl (n = 8) mice were treated with tamoxifen, and 1 month later infected with 150 PFU of JHMV. Clinical scores (left) and area under curve were calculated. All data displayed as mean with SEM. Means are of biological replicates. Clinical score significance determined using two-way ANOVA statistical test with multiple comparisons. Area under the curve significance calculated by one-way ANOVA, comparing each group to WT (B) or by Student’s t test (C). *p<0.05, ***p<0.001.

Figure 7.

Figure 7—figure supplement 1. TLR4 signals within microglial cells to limit morbidity in response to JHMV infection of the CNS.

Figure 7—figure supplement 1.

(A) Brains from R26R-EYFP; nestin-Cre mice were gated on YFP+ (left) or YFP- (right) populations and microglial markers displayed. (B) qPCR of TLR4 from unpurified splenocytes, CD11b+ MACS purified splenocytes, and CD11b+ MACS purified brain cells of tamoxifen-treated control (TLR4-fl/fl) and microglialΔTLR4 (CX3CR1CreER); TLR4-fl/fl) mice. Data represented as mean ± SEM. Means are calculated from biological replicates.