HTLV-1 pDC stimulation was TLR7 dependent. IFN-α secretion (A), TRAIL (B), and activation marker expressions CD40, CD83, CD86 (C) by HTLV-1–activated pDCs were inhibited by the use of the inhibitor of endosomal acidification (chloroquine) in a dose-response manner (0.25-1μM). TRAIL expression and activation markers (light gray histograms in B and C) compared with unstimulated pDCs (solid gray histograms) are significantly reduced by chloroquine at 0.5μM (dark gray histograms). IFN-α secretion (D) and TRAIL expression (E) by HTLV-1–activated pDCs were blocked by use of the TLR7 inhibitor (A151) in a dose-response manner. TRAIL expression (light gray histograms in E) compared with unstimulated pDC (solid gray histograms) is significantly reduced in the presence of A151 at 10μM (dark gray histograms). Data shown in each panel are representative of at least 3 independent experiments.