Sorafenib reduces lymphocyte stimulation capacity of DCs. DCs were irradiated with 30 Gy and were incubated for 5 days with 10⁵ allogenic PBMCs or CD3⁺ T cells. Thymidine incorporation was measured by a 16-hour pulse with [³H]thymidine. PBMCs or T cells without DCs were included as a control. (A) DCs were pretreated with sorafenib 48 hours before harvesting and immature as well as LPS-stimulated DCs (10³ DCs per well) were incubated with untreated PBMCs. (B) Untreated mature DCs (10³ DCs per well) were incubated with MACS isolated CD3⁺ T cells pretreated with different concentrations of sorafenib as indicated in the figure. (C) Untreated mature DCs (10³ DCs per well) were incubated with MACS isolated CD3⁺ T cells pretreated with different concentrations of sorafenib as indicated in the figure. Sorafenib was added to the cell culture medium in the same concentrations during MLR. (D) DCs were pretreated with sunitinib, stimulated with LPS, and incubated with untreated PBMCs (*P < .05, ** P < .001). (E) Induction of Her-2/neu specific primary CTL responses was analyzed using LPS activated DCs pretreated with sorafenib or sunitinib and pulsed with an HLA-A2 binding Her-2/neu-derived E75 peptide. DCs pulsed with the E75 peptide as well as the HLA-A2-positive and Her-2/neu-expressing cell line A-498 were used as targets. The HLA-A2-negative and Her-2/neu-positive cell line SKOV-3, the HLA-A2-negative and Her-2/neu-negative cell line K-562, and DCs pulsed with an irrelevant HIV-derived peptide were included as negative controls.