Figure 5.
Figure 5. Normal B cells do not rescue the impaired proliferation of iNKT cells in patients with HHV-8 MCD. (A) Experimental design. B cells from HDs were isolated by negative selection, cocultured with allogeneic B cell–depleted PBMCs from patients with HHV-8 MCD, and stimulated for 7 days with α-GalCer and IL-2. Alternatively, negative isolated B cells from patients with HHV-8 MCD were cultured with allogeneic B cell–depleted PBMCs from HDs. As controls, B cells from HDs were cultured with allogeneic and autologous B cell–depleted PBMCs from HDs; B cells from patients with HHV-8 MCD were cultured with autologous B cell–depleted PBMCs derived from patients with HHV-8 MCD. Cells were stained with CD3 and iTCR mAbs to identify iNKT cells. (B) Bar chart shows cumulative data as frequencies and median ± interquartile ranges of iNKT cells at day 7 in the PBMCs of 6 HDs and 3 patients with HHV-8 MCD. Significant P < .05, Kruskal-Wallis and Mann-Whitney tests.

Normal B cells do not rescue the impaired proliferation of iNKT cells in patients with HHV-8 MCD. (A) Experimental design. B cells from HDs were isolated by negative selection, cocultured with allogeneic B cell–depleted PBMCs from patients with HHV-8 MCD, and stimulated for 7 days with α-GalCer and IL-2. Alternatively, negative isolated B cells from patients with HHV-8 MCD were cultured with allogeneic B cell–depleted PBMCs from HDs. As controls, B cells from HDs were cultured with allogeneic and autologous B cell–depleted PBMCs from HDs; B cells from patients with HHV-8 MCD were cultured with autologous B cell–depleted PBMCs derived from patients with HHV-8 MCD. Cells were stained with CD3 and iTCR mAbs to identify iNKT cells. (B) Bar chart shows cumulative data as frequencies and median ± interquartile ranges of iNKT cells at day 7 in the PBMCs of 6 HDs and 3 patients with HHV-8 MCD. Significant P < .05, Kruskal-Wallis and Mann-Whitney tests.

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