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. 2013 Jan 6;66(3):589–597. doi: 10.1007/s12013-012-9505-4

Fig. 2.

Fig. 2

a Binding of HCV E2 protein to NIH3T3/L-SIGN. Cells were treated with E2 (thick lines) or left untreated (dotted lines) and the E2 binding was detected with mouse anti-E2 mAb and FITC-conjugated goat anti-mouse IgG by flow cytometry. b Inhibition of HCV E2 binding to NIH3T3/L-SIGN by antibodies against L-SIGN or DC-SIGN. Cells were incubated with mouse anti-L-SIGN mAb at a concentration of 4 μg/ml (II), 10 μg/ml (III) or 10 μg/ml anti-DC-SIGN mAb, and 10 μg/ml anti-L-SIGN mAb (IV) before the E2 incubation. The E2 binding was detected with goat anti-E2 Ab and FITC-conjugated rabbit anti-goat IgG in the presence or absence (I) of the antibody incubation. The percentage of marker-positive cells is indicated in each case. Data are representative of three experiments