Figure 3
Figure 3. Impaired CCL3 binding in CCR2-deficient PBMCs. Peripheral blood mononuclear cells were assayed for CCL3 binding as a measurement of CCR1/CCR5 function by flow cytometry. When comparing wild-type (A) and Ccr2−/− (B) mice, a decreased percentage of CD11b+ cells shows CCL3 binding in cells lacking CCR2; a specificity control using a CCL3-blocking antibody is shown (C). Decreased CCL3 binding was not observed in other chemokine receptor–deficient lines with intact CCR2 expression, such as Cxcr3−/− mice (D). Graphed results (E) revealed a 50% reduction in CCL3 binding in cells lacking CCR2. Bars show mean value with SD. Each point in the bar represents an individual mouse.

Impaired CCL3 binding in CCR2-deficient PBMCs. Peripheral blood mononuclear cells were assayed for CCL3 binding as a measurement of CCR1/CCR5 function by flow cytometry. When comparing wild-type (A) and Ccr2−/− (B) mice, a decreased percentage of CD11b+ cells shows CCL3 binding in cells lacking CCR2; a specificity control using a CCL3-blocking antibody is shown (C). Decreased CCL3 binding was not observed in other chemokine receptor–deficient lines with intact CCR2 expression, such as Cxcr3−/− mice (D). Graphed results (E) revealed a 50% reduction in CCL3 binding in cells lacking CCR2. Bars show mean value with SD. Each point in the bar represents an individual mouse.

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