Figure 4.
In vitro–exhausted Vγ9Vδ2 T cells have reduced effector functions. (A) Dot plots from a representative donor of surface expression of CD3. (B) Minimal previsions of TNF-α and IFN-γ cytokines after PMA/ionomycin (control), UCHT1 or OKT3 stimulation by untreated (blue) or treated (red) Vγ9Vδ2 T cells. (C) Frequency (%) of CD107a among treated (red) vs untreated (blue) Vγ9Vδ2 T cells after increasing concentrations of anti-CD3 mAb UCHT1 (round) or OKT3 (square). Positive control: PHA (10 ng/mL). n = 4. (D) Quantification of the UCHT1 or OKT3 mAb concentration (nanomolar) allowing to produce 50% of the maximal observed reactivation of untreated (blue) vs treated (red) Vγ9Vδ2 T cells. n > 3. All statistical analysis were performed using 2-way ANOVA (∗P < .05; ∗∗P < .003; ∗∗∗P < .0005; ∗∗∗∗P < .0001). mAb, monoclonal antibody; PHA, phytohemagglutinin; SSC, side scatter.

In vitro–exhausted Vγ9Vδ2 T cells have reduced effector functions. (A) Dot plots from a representative donor of surface expression of CD3. (B) Minimal previsions of TNF-α and IFN-γ cytokines after PMA/ionomycin (control), UCHT1 or OKT3 stimulation by untreated (blue) or treated (red) Vγ9Vδ2 T cells. (C) Frequency (%) of CD107a among treated (red) vs untreated (blue) Vγ9Vδ2 T cells after increasing concentrations of anti-CD3 mAb UCHT1 (round) or OKT3 (square). Positive control: PHA (10 ng/mL). n = 4. (D) Quantification of the UCHT1 or OKT3 mAb concentration (nanomolar) allowing to produce 50% of the maximal observed reactivation of untreated (blue) vs treated (red) Vγ9Vδ2 T cells. n > 3. All statistical analysis were performed using 2-way ANOVA (∗P < .05; ∗∗P < .003; ∗∗∗P < .0005; ∗∗∗∗P < .0001). mAb, monoclonal antibody; PHA, phytohemagglutinin; SSC, side scatter.

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