Figure 5

Figure 5

Macrophages lacking Cxcr3.3 show an enhanced recruitment to sites of infection, toward Cxcl11aa, and to sites of mechanical damage. Significantly fewer cells were recruited to the hindbrain ventricle in cxcr3.2–/– at 3 hpi with Mm and more macrophages were recruited to the same site in cxcr3.3–/– compared to WT controls (A and B). The same trend was observed when 1 nl of Cxcl11aa protein (10 ng/ml) was injected in the same experimental setup (C and D). To assess macrophage recruitment to sites of injury, we used the tail‐amputation model and observed enhanced recruitment of macrophages in cxcr3.3–/– larvae and attenuated recruitment of macrophages in cxcr3.2–/– relative to WT at 4 h postamputation (E and F). The PBS‐injected control group combines WT, cxcr3.2, and cxcr3.3 mutants and shows no cell recruitment at 3 hpi. In all cases, statistical analyses were done with pooled data of 3 independent replicates (20–30 larvae per group each). A Kruskal‐Wallis test was used to assess significance (^*P ≤ 0.05, ^***P ≤ 0.001, ^****P ≤ 0.0001) and data are shown as mean ± sem