Figure 4
SD-4 on CTCL cells or PBMCs of patients with SS inhibits their anti–CD3 response following binding to DC-HIL. HuT-78 (A), HH cells (B), or PBMCs (C-D) from 2 patients with SS (Pt. 2 and Pt. 3A with Vβ+ cells at 98%, in which SD-4+ cells were 94%) were cultured with immobilized anti–CD3 Ab (increasing doses) plus 5 μg/mL DC-HIL-Fc (●) or control Ig (○). Activation was measured by IL-2 production for the HuT-78 cells (A) and PBMCs (C), by the frequency of CD69+ cells as a percentage for the HH line (B), or by 3H-thymidine (TdR) incorporation (D) as mean (± SD) for n = 3 experiments.

SD-4 on CTCL cells or PBMCs of patients with SS inhibits their anti–CD3 response following binding to DC-HIL. HuT-78 (A), HH cells (B), or PBMCs (C-D) from 2 patients with SS (Pt. 2 and Pt. 3A with Vβ+ cells at 98%, in which SD-4+ cells were 94%) were cultured with immobilized anti–CD3 Ab (increasing doses) plus 5 μg/mL DC-HIL-Fc (●) or control Ig (○). Activation was measured by IL-2 production for the HuT-78 cells (A) and PBMCs (C), by the frequency of CD69+ cells as a percentage for the HH line (B), or by 3H-thymidine (TdR) incorporation (D) as mean (± SD) for n = 3 experiments.

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