Fig. 6

Agonists of liver-X-receptor (LXR) α/β signaling promote anti-inflammatory DAM and Aβ phagocytic activity in microglia. a Experimental design: 6–7 mo 5xFAD mice (females, n = 4/group) received either vehicle (20% DMSO) or a LXR α/β agonist T0901317 (30 mg/kg i.p. daily × 2 weeks) after which acutely isolated CNS immune cells were assessed for flow cytometric immuno-phenotyping as well as flow cytometric assays of fluorescent fibrillar Aβ. b, c CD11b⁺CD45^low CNS immune cells were assessed for CD11c expression. A comparison of CD11c expression in 5xFAD mice (blue) and WT mice (red) is shown. Gating threshold for CD11c is shown in (c). d, e A comparison of CD44 and CXCR4 expression profiles within CD11c⁺ DAM acutely isolated from vehicle-treated or T0901317-treated 5xFAD mice. Relative proportions of each subset (of all CD11b⁺CD45^lowCD11c⁺ DAM) are shown. Yellow represents anti-inflammatory DAM, Magenta represents pro-inflammatory DAM and Brown represents double positive cells. A quantitative analysis of various subsets of CD11c + DAM in vehicle-treated and T0901317-treated mice is shown in (e). f Comparison of ability of acutely isolated CD11b⁺CD45^low microglia (from vehicle-treated and T0901317-treated mice) to phagocytose fluorescent Aβ42 fibrils. *p < 0.05, **p < 0.01, ***p < 0.005