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. 2017 Dec 8;141(1):132–147. doi: 10.1093/brain/awx315

Figure 6.

Figure 6

CD11c+ microglial ERβ expression is not necessary for neuroprotection in EAE. (A) Diagram for creating CD11c+ microglia-CKO using BMC. Briefly, CD45.1 wild-type mice were used as donors for bone marrow cells, and CD45.2 wild-type (WT→WT) or CKO (WT→CKO) were used as irradiated recipients. Each genotype was separated into two groups and received either vehicle or ERβ-ligand treatment (tx), EAE was induced and mice were scored for EAE severity. (B) ERβ-ligand treated wild-type (WT→WT-ERβ, blue solid) EAE mice had significantly better scores compared to vehicle treated wildtype (WT→WT-V, blue clear) EAE mice, *P (WT→WT-V versus WT→WT-ERβ) = 0.0188. Similarly, ERβ-ligand treated CKO (WT→CKO-ERβ, black solid) EAE mice also had significantly better scores compared to vehicle treated conditional knockout (WT→CKO-V, black clear) EAE mice, **P (WT→CKO-V versus WT→CKO-ERβ) = 0.0077. Detailed EAE statistics are in Supplementary Tables 1 and 2. Quantitative analysis of (C) NF200+ axonal count, (D) βAPP+ axonal count, (E) MBP+ myelin intensity, and (F) MHCII expression on Iba1+ myeloid derived cells (percentage) in dorsal white matter of the spinal cord. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001. Data are representative of two repeated experiments.