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. 2014 Dec 15;125(1):365–378. doi: 10.1172/JCI66771

Figure 5. CXCR3 deficiency and CXCR3 antagonism enhance microglial phagocytosis of FAM-Aβ and reduce the production of TNF-α in vitro.

Figure 5

(A) Primary WT and Cxcr3–/– microglia (CD68, red signal) were incubated with or without 0.7 μM FAM-Aβ for 1 hour. Scale bar: 20 μm. (B) A phagocytosis assay revealed a significant increase of FAM-Aβ uptake in Cxcr3–/– compared with WT microglia. mCXCL9 and mCXCL10 (each 250 ng/ml) treatment of WT and Cxcr3–/– microglia diminished phagocytosis in WT but not in Cxcr3–/– cells. (C) Reduced TNF-α concentration in the cell supernatants of Aβ-stimulated Cxcr3–/– microglia cultures. (D) Functional blocking of CXCR3 with an antagonist enhances microglial phagocytosis to levels equal to those found in CXCR3-deficient microglia (CXCR3 antagonist ≥ 100 nM). (E) Analysis of the TNF-α level in CXCR3 antagonist–treated WT microglia exhibits a reduction of TNF-α secretion below WT control level when stimulated with Aβ. Data are shown as mean ± SEM from 3 to 5 individual experiments; *P < 0.05; **P < 0.01; ***P < 0.001 (1-way ANOVA, Dunn’s post hoc test).