Figures & data
Figure 1. Attenuated measles virus (MV) antitumoral virotherapy activates myeloid and plasmacytoid dendritic cells, notably their capacity to cross-present tumor-associated antigens (TAA): MV preferentially infects tumor cells due to their overexpression of CD46. MV-infected tumor cells are lysed. They induce maturation of myeloid DC, mainly by DAMP expression (HSP70, gp96, IFNα, IFNβ, HMGB1, IL-6, IL-8), and maturation of plasmacytoid DC, mainly by MV single-strand RNA, a pathogen associated molecular pattern (PAMP) that triggers TLR7 expressed by pDC. DC internalized fragments of MV-infected tumor cells and cross-present TAA to specific CD8+ T cells. It has been demonstrated for myeloid DC that this cross-presentation can result in cross-priming, whereas this has not been demonstrated for pDC. pDC also produce large amount of IFN-α in response to tumor infected cells. This figure has been made using Servier Medical Art.
![Figure 1. Attenuated measles virus (MV) antitumoral virotherapy activates myeloid and plasmacytoid dendritic cells, notably their capacity to cross-present tumor-associated antigens (TAA): MV preferentially infects tumor cells due to their overexpression of CD46. MV-infected tumor cells are lysed. They induce maturation of myeloid DC, mainly by DAMP expression (HSP70, gp96, IFNα, IFNβ, HMGB1, IL-6, IL-8), and maturation of plasmacytoid DC, mainly by MV single-strand RNA, a pathogen associated molecular pattern (PAMP) that triggers TLR7 expressed by pDC. DC internalized fragments of MV-infected tumor cells and cross-present TAA to specific CD8+ T cells. It has been demonstrated for myeloid DC that this cross-presentation can result in cross-priming, whereas this has not been demonstrated for pDC. pDC also produce large amount of IFN-α in response to tumor infected cells. This figure has been made using Servier Medical Art.](/cms/asset/db78187d-7756-4721-833a-6ac8cde2581f/koni_a_10924212_f0001.gif)