Figure 4. TREM2 deficiency reduces antibody‐mediated amyloid plaque clearance.

• A
  BMDM from wt or Trem2 ko mice were cultured on APP/PS1 mice brain cryosections incubated with or without mAb11 (1 μg/ml) or an isotype control (IC; 1 μg/ml) for 24 h. Sections were then probed with methoxy‐X04. Scale bar, 500 μm.
• B
  The amyloid plaque load was quantified from the entire sagittal section. Sections incubated with medium (no cell) were set as baseline. (n = 6, ± SEM; two‐way ANOVA, interaction P < 0.0001, genotype P < 0.0001, treatment P < 0.0001; Tukey's multiple comparisons tests; wt vs. ko for the following conditions: no antibody P = 0.0304, IC P = 0.0049, mAb11 P = 0.0212; wt: IC vs. wt: mAb11 P = 0.0008; ko: IC vs. ko: mAb11 P = 0.0001).
• C, D
  Equal numbers of wt and Trem2 ko BMDM were added, and cell numbers were analyzed after termination of experiments by quantifying the CD68‐positive cells on top of the sections. (n = 4, ± SEM; t‐test; n.s., non‐significant, P = 0.5004). Scale bar, 200 μm.
• E
  Aβ was extracted by urea buffer from replicate slices of the experiment shown in (A), and total Aβ was identified by Western blotting.

Source data are available online for this figure.