Figure 6.
Figure 6. CD38/CD31 crosstalk cooperates with CD100/plexin-B1 in inducing survival of B-CLL cells. CD38+ B-CLL cells (patients nos. 1, 4, 6, and 7) were exposed to CD38- and IL-2–mediated signals for 5 days to induce the appearance of a highly CD100+ subset. The cells were then collected, washed to remove anti-CD38 mAb and IL-2, and plated (1) on a layer of NIH/Plex-B1; (2) on control wild-type NIH-3T3 cells; (3) or in complete medium; or were maintained in the presence of anti-CD38 mAb and IL-2. Viability was tested after 72 hours by annexin-V staining (A), while proliferation was measured by PI staining (B). The percentages of annexin-V+ cells were derived from cells in the R1 and R2 gates (see Figure 5). The specificity of the system was confirmed by blocking the availability of the plexin-B1 ligand using the specific B6-9 mAb. The irrelevant JAS mAb was used as the control. Data are the mean values obtained using B-CLL cells from 4 patients in 2 separate experiments; error bars represent the SD.

CD38/CD31 crosstalk cooperates with CD100/plexin-B1 in inducing survival of B-CLL cells. CD38+ B-CLL cells (patients nos. 1, 4, 6, and 7) were exposed to CD38- and IL-2–mediated signals for 5 days to induce the appearance of a highly CD100+ subset. The cells were then collected, washed to remove anti-CD38 mAb and IL-2, and plated (1) on a layer of NIH/Plex-B1; (2) on control wild-type NIH-3T3 cells; (3) or in complete medium; or were maintained in the presence of anti-CD38 mAb and IL-2. Viability was tested after 72 hours by annexin-V staining (A), while proliferation was measured by PI staining (B). The percentages of annexin-V+ cells were derived from cells in the R1 and R2 gates (see Figure 5). The specificity of the system was confirmed by blocking the availability of the plexin-B1 ligand using the specific B6-9 mAb. The irrelevant JAS mAb was used as the control. Data are the mean values obtained using B-CLL cells from 4 patients in 2 separate experiments; error bars represent the SD.

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