Tumor-infiltrating dendritic cell precursors recruited by a beta-defensin contribute to vasculogenesis under the influence of Vegf-A.

摘要: The involvement of immune mechanisms in tumor angiogenesis is unclear. Here we describe a new mechanism vasculogenesis mediated by dendritic cell (DC) precursors through the cooperation β-defensins and vascular endothelial growth factor-A (Vegf-A). Expression mouse β-defensin-29 recruited DC to tumors enhanced vascularization presence increased Vegf-A expression. A leukocyte population expressing markers was uncovered human ovarian carcinomas coexpressing β-defensins. Tumor-infiltrating DCs migrated vessels independently assembled neovasculature vivo. Bone marrow–derived underwent endothelial-like differentiation ex vivo, blood promoted high levels Vegf-A. We show that cooperate promote carrying out distinct tasks: chemoattract CCR6, whereas primarily induces their specialization migration vessels, which Vegf receptor-2.