Figure 2.
Figure 2. Imatinib restores PDC function in vivo. (A) PBMCs isolated from healthy volunteers or patients with CML treated with imatinib were analyzed by flow cytometry after 3-color staining with a combination of FITC-labeled monoclonal antibodies against lineage markers (CD3, CD14, CD16, CD19, and CD56), phycoerythrin (PE)-labeled anti-CD11c and phycoerythrin-cyanin 5.1 (PC5)-labeled anti-ILT3. Two distinct populations of lin-/ILT3+ cells were observed with respect to the expression of CD11c with the phenotypes of lin-/CD11c+/ILT3+ (myeloid DCs) and lin-/CD11c-/ILT3+ (PDCs). Examples of results obtained from more than 15 healthy volunteers (left panel), 7 patients with CML in complete cytogenetic or molecular remission after imatinib treatment (middle panel), and 2 patients with CML not reaching cytogenetic or molecular remission after imatinib treatment (right panel). P = not significant for comparison of PDC numbers between healthy donors (left panel) and patients with CML in complete cytogenetic or molecular remission after imatinib treatment (middle panel). Percentages in upper left quadrants denote PDCs; in upper right quadrants, myeloid DCs. (B) IFN-α secretion by PDCs from healthy donors and patients with CML receiving imatinib treatment following stimulation with HSV. Cells were stimulated with HSV without any additional cytokine. Supernatants were harvested after 48 hours of stimulation. IFN-α secretion was analyzed by ELISA. Concentrations obtained from 104 PDCs are represented as the mean and SEM of IFN-α secretion obtained from 5 healthy donors, 5 patients with CML in complete cytogenetic or molecular remission after imatinib treatment, and 2 patients with CML not reaching cytogenetic or molecular remission after imatinib treatment. P = not significant for comparison of IFN-α secretion between healthy donors and patients with CML in complete cytogenetic or molecular remission after imatinib treatment. Control conditions that were not stimulated with HSV did not contain detectable or significant amounts of IFN-α.

Imatinib restores PDC function in vivo. (A) PBMCs isolated from healthy volunteers or patients with CML treated with imatinib were analyzed by flow cytometry after 3-color staining with a combination of FITC-labeled monoclonal antibodies against lineage markers (CD3, CD14, CD16, CD19, and CD56), phycoerythrin (PE)-labeled anti-CD11c and phycoerythrin-cyanin 5.1 (PC5)-labeled anti-ILT3. Two distinct populations of lin-/ILT3+ cells were observed with respect to the expression of CD11c with the phenotypes of lin-/CD11c+/ILT3+ (myeloid DCs) and lin-/CD11c-/ILT3+ (PDCs). Examples of results obtained from more than 15 healthy volunteers (left panel), 7 patients with CML in complete cytogenetic or molecular remission after imatinib treatment (middle panel), and 2 patients with CML not reaching cytogenetic or molecular remission after imatinib treatment (right panel). P = not significant for comparison of PDC numbers between healthy donors (left panel) and patients with CML in complete cytogenetic or molecular remission after imatinib treatment (middle panel). Percentages in upper left quadrants denote PDCs; in upper right quadrants, myeloid DCs. (B) IFN-α secretion by PDCs from healthy donors and patients with CML receiving imatinib treatment following stimulation with HSV. Cells were stimulated with HSV without any additional cytokine. Supernatants were harvested after 48 hours of stimulation. IFN-α secretion was analyzed by ELISA. Concentrations obtained from 104 PDCs are represented as the mean and SEM of IFN-α secretion obtained from 5 healthy donors, 5 patients with CML in complete cytogenetic or molecular remission after imatinib treatment, and 2 patients with CML not reaching cytogenetic or molecular remission after imatinib treatment. P = not significant for comparison of IFN-α secretion between healthy donors and patients with CML in complete cytogenetic or molecular remission after imatinib treatment. Control conditions that were not stimulated with HSV did not contain detectable or significant amounts of IFN-α.

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