Figure 4. Cell subsets and IL-10.

A. HCV-specific (to Pools 1 (Core) and 2 (NS3)), C. albicans-specific, and PHA-induced IL-10 SFU/10⁶ PBMC in unfractionated PBMC and CD8⁺ T-cell-depleted PBMC in 6 chronic HCV patients. Depleted subset SFU were corrected for changes in T-cell frequency by multiplying by [%CD3_PBMC}/[%CD3_CD8−]. B. Summed HCV-specific IL-10 SFU/10⁶ PBMC to 12 pools of 15mer overlapping peptides spanning Core, NS3-NS5 with unfractionated and CD4⁺ T-cell-depleted PBMC in 17 chronic HCV patients. C. IL-10 secretion measured by cytokine bead array (expressed in log IL-10 pg/ml) in 24 hour unstimulated and PMA/ionomycin stimulated cultures of unfractionated PBMC, bead-selected CD4⁺CD25⁺ and CD4⁺CD25⁻ subsets in 5 chronic HCV patients. D. Correlation of frequency of peripheral CD4⁺CD25⁻FITC⁺ T-cells and IL-10 SFU/10⁶ PBMC in 59 chronic HCV patients. E. CD4⁺CD25^hi and CD4⁺foxp3⁺ T-cell frequency in acute HCV patients. CD25⁺ cutoff was defined by 99.9% isotype in the lymphoid gate, while CD25^hi was defined by 99.9% of CD8⁺ T-cells. An example of the gating strategy for CD4⁺CD25^hi population and CD4⁺foxp3⁺ gating is shown in Supplementary Figure 1. For 3 AR and 2 AC subjects CD4⁺CD25^hi (grey bars) and CD4⁺foxp3⁺ (white bars) are plotted relative to IL-10 SFU/10⁶ PBMC (black line).