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. 2017 Dec 4;14:238. doi: 10.1186/s12974-017-1015-2

Fig. 3.

Fig. 3

Inflammatory monocyte infiltration during acute infection requires CCR2. Brain-infiltrating leukocytes were collected from C57Bl/6 mice (WT; a, c) and CCR2−/− mice (b, d) at 18 hpi. Flow plots in (ad) show cells in a CD45+ parent gate. The number of inflammatory monocytes (IM; CD45hiCD11b+Gr1++1A8), neutrophils (N; CD45hiCD11b++Gr1+1A8+), and microglia (M; CD45midCD11bmidGr11A8) was measured by flow cytometry. The percent of inflammatory monocytes, neutrophils, and microglia in the CD45+ population is shown as mean ± 95%CI calculated from nine mice per genotype in three separate experiments (3 × 3) (e). Data were analyzed by Dunnett’s method. No difference in microglia was observed, but neutrophils were significantly increased in CCR2−/− mice (P = 0.0012 vs WT). Notably, the absence of CCR2 robustly inhibited inflammatory monocyte infiltration (P = 0.0004 vs WT). **P < 0.001