Figure 7

Immune system identity predicts CA1 neuronal protection or injury.

BILs were isolated using a 1.080 g/mL Percoll interface at 18 hpi from mice in the 4 bone marrow reconstitution groups described in Supplemental Figure 1 and phenotyped by flow cytometry. The number of SJL inflammatory monocytes (CD45.2⁺CD11b⁺Gr1⁺) and B10.S inflammatory monocytes (CD45.1⁺CD11b⁺Gr1⁺) were measured in each of the 4 transplant groups (A). SJL mice reconstituted with a B10.S immune system (C) had as many inflammatory monocytes as B10.S transplant controls (B), while B10.S mice reconstituted with an SJL immune system (E) exhibited the same low level inflammatory monocyte response observed in SJL transplant controls (D). Eight weeks after bone marrow reconstitution mice were infected with TMEV. Hippocampal sections were prepared at 7 dpi and injury to CA1 was quantified as in Figure 2. SJL mice reconstituted with a B10.S immune system (B10.S→SJL) (H) showed hippocampal damage that was indistinguishable from B10.S transplant controls (B10.S→B10.S) (F). Likewise, B10.S mice reconstituted with an SJL immune system (SJL→B10.S) (I) showed neuron preservation that was the same as SJL transplant controls (SJL→SJL) (G). Measurements for individual animals are shown in the scatter plot (J). Dot plots are representative of at least 4 mice in 2 separate experiments. The bar graph in A shows mean ± 95% CI. The error bars in J are centered on the mean hippocampal injury score and show the 95% CI for each group. The scale bar in I is 50 μm and refers to F–I. The pathology is representative of at least 10 mice per condition in 2 separate experiments.