We are analyzing https://link.springer.com/article/10.1007/s00262-006-0234-7.

Title:
Vascular endothelial growth factor inhibits the function of human mature dendritic cells mediated by VEGF receptor-2 | Cancer Immunology, Immunotherapy
Description:
Dendritic cells (DCs) are the most potent antigen-presenting cells and play a central role in the host-antitumor immunity. Since it has been reported that vascular endothelial growth factor (VEGF) inhibits the functional maturation of immature-DCs and impairs DC differentiation, it is important to elucidate the mechanisms of VEGF-induced DC-dysfunction. To investigate the effects of VEGF against human mature DCs, we investigated how VEGF affects mature DCs with regards to phenotype, induction of apoptosis, IL-12(p70) production and the antigen-presenting function evaluated by allogeneic mixed leukocyte reaction (allo-MLR). We generated monocyte-derived DCs matured with lipopolysaccharide, OK-432 or pro-inflammatory cytokine cocktails. As a result, VEGF treatment did not alter the mature DCs with regard to phenotype, IL-12(p70) production and induction of apoptosis. As a novel and important finding, VEGF inhibited the ability of mature DCs to stimulate allogeneic T cells. Furthermore, this VEGF-induced DC dysfunction was mainly mediated by VEGF receptor-2 (VEGF R2). These observations were confirmed by the findings that the VEGF-induced DC dysfunction was recovered by anti-human VEGF neutralizing mAb or anti-human VEGF R2 blocking mAb, and that placenta growth factor (PlGF), VEGF R1-specific ligand, did not have any effect against mature DCs. Some modalities aiming at reversing mature-DC dysfunction induced by VEGF will be needed in order to induce the effective antitumor immunity.
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Keywords {🔍}

cas, google, scholar, pubmed, article, cells, dendritic, growth, factor, endothelial, cancer, vascular, vegf, cell, immunol, carbone, gabrilovich, human, mature, function, inhibits, receptor, dcs, maturation, nadaf, differentiation, privacy, cookies, content, kono, functional, production, monocytederived, access, immune, expression, defective, res, blood, information, publish, search, immunotherapy, mediated, takahashi, dysfunction, antitumor, angiogenesis, clin, martin,

Topics {✒️}

yoshihiko kawaguchi & hideki fujii month download article/chapter tumor-infiltrating dendritic cells s-100 protein-positive cells pro-inflammatory cytokine cocktails monocyte-derived dendritic cells tumor-induced immune suppression vegf-induced dc-dysfunction vegf-induced dc dysfunction vegf r1-specific ligand placenta growth factor potent antigen-presenting cells dendritic cells derived human tumors inhibits antigen-presenting function evaluated dendritic cells induced article cancer immunology full article pdf dendritic cell differentiation related subjects dendritic cells grown dendritic cells stimulated human mature dcs nuclear factor-kappa cross-priming capability privacy choices/manage cookies antitumor immune responses decreased antigen presentation dendritic cell induction immature myeloid cells cell surface marker defective antigen presentation t-cell activation tumor-bearing hosts tumor-bearing mice tumor-bearing animals tumor rejection peptide host-antitumor immunity effective antitumor immunity ohm je impairs dc differentiation hemopoietic progenitor cells t-zone histiocytes inducible b7 expression effective antigen carriers article mimura antigen-presenting function european economic area myeloma-specific killer multiple hematopoietic lineages

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         description:Dendritic cells (DCs) are the most potent antigen-presenting cells and play a central role in the host-antitumor immunity. Since it has been reported that vascular endothelial growth factor (VEGF) inhibits the functional maturation of immature-DCs and impairs DC differentiation, it is important to elucidate the mechanisms of VEGF-induced DC-dysfunction. To investigate the effects of VEGF against human mature DCs, we investigated how VEGF affects mature DCs with regards to phenotype, induction of apoptosis, IL-12(p70) production and the antigen-presenting function evaluated by allogeneic mixed leukocyte reaction (allo-MLR). We generated monocyte-derived DCs matured with lipopolysaccharide, OK-432 or pro-inflammatory cytokine cocktails. As a result, VEGF treatment did not alter the mature DCs with regard to phenotype, IL-12(p70) production and induction of apoptosis. As a novel and important finding, VEGF inhibited the ability of mature DCs to stimulate allogeneic T cells. Furthermore, this VEGF-induced DC dysfunction was mainly mediated by VEGF receptor-2 (VEGF R2). These observations were confirmed by the findings that the VEGF-induced DC dysfunction was recovered by anti-human VEGF neutralizing mAb or anti-human VEGF R2 blocking mAb, and that placenta growth factor (PlGF), VEGF R1-specific ligand, did not have any effect against mature DCs. Some modalities aiming at reversing mature-DC dysfunction induced by VEGF will be needed in order to induce the effective antitumor immunity.
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