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. 2020 Jun 23;9:e54590. doi: 10.7554/eLife.54590

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© 2020, McKinsey et al

This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.

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Figure 2. — (A) Cartoon depicting the subsets of brain macrophage populations that were analyzed in P2ry12-CreER; Rosa26^Ai14 mice. D-BAMs, SD-BAMs, CP-BAMs = dural, subdural, choroid plexus border-associated macrophages. PVMs = perivascular macrophages. Adapted, with permission, from Van Hove et al., 2019. (B) Analysis of P2ry12-CreER; Rosa26^Ai14 recombination in SMA-adjacent LYVE1+ perivascular macrophages. No recombination was seen in perivascular macrophages, unlike Cx3CR1-CreER; Rosa26^Ai14 mice (see Figure 2—figure supplement 1). (C) Analysis of recombination in LYVE1+ pial macrophages. ERTR7 expression delineates pial boundaries. (D) Analysis of recombination in SMA-adjacent CD206+ perivascular macrophages. (E) Analysis of recombination in IBA1+ macrophages of the choroid plexus. (F) Whole-mount cerebral cortex and dura, immunostained for CD206. (G) Whole-mount cerebral cortex and dura, immunostained for LYVE1. Weakly red cells in pial images are microglia in deeper focal planes. (H–I) Quantification of recombination in CD206+ (H) and LYVE1+ (I) macrophages in the parenchymal, pial and dural spaces. (J) Quantification of recombination in IBA1+ macrophages of the choroid plexus. Error bars = SEM. Scale bars = 100 µm (B–G).

Figure 2—source data 1. Analysis of P2ry12-CreER recombination in brain macrophage populations.

elife-54590-fig2-data1.xlsx^{(10.3KB, xlsx)}

Figure 2—figure supplement 1. — (A) Cartoon depicting the subsets of brain macrophage populations that were analyzed in P2ry12-CreER; Rosa26^Ai14 mice. D-BAMs, SD-BAMs, CP-BAMs = dural, subdural, choroid plexus border-associated macrophages. PVMs = perivascular macrophages. Adapted, with permission, from Van Hove et al., 2019. (B) Analysis of P2ry12-CreER; Rosa26^Ai14 recombination in SMA-adjacent LYVE1+ perivascular macrophages. No recombination was seen in perivascular macrophages, unlike Cx3CR1-CreER; Rosa26^Ai14 mice (see Figure 2—figure supplement 1). (C) Analysis of recombination in LYVE1+ pial macrophages. ERTR7 expression delineates pial boundaries. (D) Analysis of recombination in SMA-adjacent CD206+ perivascular macrophages. (E) Analysis of recombination in IBA1+ macrophages of the choroid plexus. (F) Whole-mount cerebral cortex and dura, immunostained for CD206. (G) Whole-mount cerebral cortex and dura, immunostained for LYVE1. Weakly red cells in pial images are microglia in deeper focal planes. (H–I) Quantification of recombination in CD206+ (H) and LYVE1+ (I) macrophages in the parenchymal, pial and dural spaces. (J) Quantification of recombination in IBA1+ macrophages of the choroid plexus. Error bars = SEM. Scale bars = 100 µm (B–G).

Figure 2—source data 1. Analysis of P2ry12-CreER recombination in brain macrophage populations.

elife-54590-fig2-data1.xlsx^{(10.3KB, xlsx)}