Vγ9Vδ2-T–cell dysfunction is reversible upon ex vivo activation and expansion. Vγ9Vδ2-T cells from CLL patients (n = 8), with previously confirmed impaired function, and Vγ9Vδ2-T cells from HCs (n = 4) were sorted by FACS and subsequently cultured for 2 weeks with phosphoantigen-expressing moDCs in the presence of IL-7 and IL-15. Alternatively, Vγ9Vδ2-T cells (CLL, n = 4; HC, n = 4) were generated from CD19-depleted PBMCs by culture in the presence of ABPs and IL-2 for 2 weeks. (A) Expansion factor of Vγ9Vδ2-T cells calculated by dividing the amount of Vγ9Vδ2-T cells after a 2-week culture with allogeneic HC-derived moDCs (Allo-moDC) or autologous moDCs (Auto-moDC) by the number of Vγ9Vδ2-T cells at the start of culture. Cytokine production (B) and CD107a expression (C) by CLL-derived and HC-derived Vγ9Vδ2-T cells after culture with autologous moDCs. Vγ9Vδ2-T cells were cocultured with ABP-pretreated Daudi cells for 16 to 18 hours, and brefeldin A and GolgiStop were added during the last 6 hours of coculture. Granzyme B (D) and CD160 (F) expression on Vγ9Vδ2-T cells before and after culture with autologous moDCs. (E) Distribution of differentiation subsets within Vγ9Vδ2-T cells after culture with autologous moDCs based on CD27 and CD45RA expression. Data are mean and SEM. **P < .01, paired t test (D,F). T_CM, CD27⁺CD45RA⁻; T_EM, CD27⁻CD45RA⁻; T_EMRA, CD27⁻CD45RA⁺; T_N, CD27⁺CD45RA⁺.