Cell-free HTLV-1 virions induced TRAIL and activation marker expression by pDCs. (A) Purified pDCs were cultured in the absence (solid gray histograms) or presence of several concentrations of HTLV-1 (p19-equivalent, open gray histograms), and membrane TRAIL expression was measured by FACS. (B) Inhibition of membrane TRAIL expression by pDC activated by HTLV-1 virions (light gray histograms) by the use of HTLV-1 blockers (dark gray histograms) such as blocking HTLV-1 envelope antibody (anti-gp46, left) and sera containing blocking HTLV-1 antibodies from HTLV patients (Serum 1 and Serum 2, middle) and healthy donor serum (HD serum) as negative control (right). (C) Kinetics of expression of TRAIL by HTLV-1–stimulated pDCs (300 ng/mL p19-equivalent) compared with unstimulated pDCs. (D) Inhibition of activation markers expression (CD40, CD83, CD86) and chemokine receptors (CXCR4, CCR5) on pDCs stimulated by HTLV-1 virions (light gray histograms) with the use of HTLV-1 blockers (sera from infected HTLV patients and anti-gp46; dark gray histograms). (E) Apoptosis assay (annexin V/Topro-3 staining) of unstimulated (Unst pDC) and HTLV-1–activated pDCs (pDC + HTLV-1) in the presence of CD4⁺CD3⁺DR5⁻ or CD4⁺CD3⁺DR5⁺ T-cell target (ratio 1:2). Data shown in each panel are representative of at least 3 independent experiments.