Figure 5
Figure 5. Inhibition of pML cell invasion by AMD3100 in vivo. Infiltration of pML cells to the liver (A) and lung (B) was inhibited by AMD3100 treatment. SCID mice inoculated with pML cells (5 × 102, 5 × 103, and 5 × 104 cells/mice) were treated with either AMD3100 (AMD treated) or PBS (untreated) for 3 weeks (5 times per week) through intraperitoneal injection. Infiltration of pML cells that contain the HTLV-I Tax gene into liver and lung tissues was examined using quantitative real-time PCR. The relative copy number of Tax genome of the group (inoculated with 5 × 102, 5 × 103, and 5 × 104 pML cells) was represented by the ratio to the copy number of β-actin in liver (A) and lung (B) tissues. The ratio of Tax-positive mice/total number of mice was represented on the right side of each bar (mean ± SE).

Inhibition of pML cell invasion by AMD3100 in vivo. Infiltration of pML cells to the liver (A) and lung (B) was inhibited by AMD3100 treatment. SCID mice inoculated with pML cells (5 × 102, 5 × 103, and 5 × 104 cells/mice) were treated with either AMD3100 (AMD treated) or PBS (untreated) for 3 weeks (5 times per week) through intraperitoneal injection. Infiltration of pML cells that contain the HTLV-I Tax gene into liver and lung tissues was examined using quantitative real-time PCR. The relative copy number of Tax genome of the group (inoculated with 5 × 102, 5 × 103, and 5 × 104 pML cells) was represented by the ratio to the copy number of β-actin in liver (A) and lung (B) tissues. The ratio of Tax-positive mice/total number of mice was represented on the right side of each bar (mean ± SE).

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