Figure 3
Figure 3. HIV envelope-induced killing of Vγ2Vδ2 T cells depends on α4β7 and CCR5. (A-B) Vγ2Vδ2 T cells were stained with fluoresceine conjugated HIV gp120 (green) and Vδ2 mAb (red) and viewed under a confocal microscope (A) or analyzed with flow cytometry (B). (C) Vγ2Vδ2 T cells were stained with the fluorescein-conjugated HIV gp120 in the absence or presence of soluble CD4, and then analyzed with flow cytometry. (D) Vγ2Vδ2 T cells were incubated with Maraviroc (1μM), MAdCAM1 (20 μg/mL), or both for 1 hour before staining with HIV gp120. (E) Vγ2Vδ2 T cells were incubated with specific antibodies against CCR5, β7 or α4 (20 μg/mL) for 30 minutes before staining with HIV gp120. (F) Cell death was evaluated after Vγ2Vδ2 T cells were incubated with soluble HIV gp120 protein (CN54, 10 μg/mL) in the absence or presence of blocking reagents for α4β7 and CCR5. (G-J) Vγ2Vδ2 T cells were cultured in the absence or presence of retinoic acid. The expression of β7 (G) and CCR5 (H), the binding of gp120 (I), and gp120-induced cell death (J) were examined as previously described. Data are representative of 3 independent experiments (error bars, SD).

HIV envelope-induced killing of Vγ2Vδ2 T cells depends on α4β7 and CCR5. (A-B) Vγ2Vδ2 T cells were stained with fluoresceine conjugated HIV gp120 (green) and Vδ2 mAb (red) and viewed under a confocal microscope (A) or analyzed with flow cytometry (B). (C) Vγ2Vδ2 T cells were stained with the fluorescein-conjugated HIV gp120 in the absence or presence of soluble CD4, and then analyzed with flow cytometry. (D) Vγ2Vδ2 T cells were incubated with Maraviroc (1μM), MAdCAM1 (20 μg/mL), or both for 1 hour before staining with HIV gp120. (E) Vγ2Vδ2 T cells were incubated with specific antibodies against CCR5, β7 or α4 (20 μg/mL) for 30 minutes before staining with HIV gp120. (F) Cell death was evaluated after Vγ2Vδ2 T cells were incubated with soluble HIV gp120 protein (CN54, 10 μg/mL) in the absence or presence of blocking reagents for α4β7 and CCR5. (G-J) Vγ2Vδ2 T cells were cultured in the absence or presence of retinoic acid. The expression of β7 (G) and CCR5 (H), the binding of gp120 (I), and gp120-induced cell death (J) were examined as previously described. Data are representative of 3 independent experiments (error bars, SD).

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