Event Abstract Back to Event Lcn2 secreted from DCs induces CD8+ T-cell apoptosis, it is involved in T-cell priming, and upon DCs immunisation triggers a Th1 phenotype Melanie Floderer1, Michaela Prchal2 and Caterina Vizzardelli1* 1 St.Anna Children's Cancer Research Institute, Tumour Immunology, Austria 2 Institute of Pharmacology and Toxicology, University of Veterinary Medicine, Vienna, Dept for Biomedical Science, Austria Lipocalin 2 is expressed by dendritic cells during the late phases of Dex and LPS maturation. DCs are professional antigen presenting cells capable of regulating immunity. Besides the classical understanding concerning mouse DC subsets, new studies are suggesting that DCs follow a multi-stage differentiation programme after encountering danger signals, which facilitates the fine-tuning of the immune responses. Tolerance maintenance, immune-stimulation and immune-suppression are time dependent functions of the DCs. LCN2 is active in defence against bacteria via capturing of iron, and it is involved in autocrine apoptosis of T-cells. In order to understand the function of LCN2 in the DC/T-cell interaction, we stimulated mouse bone marrow Lcn2-/- or wild type DCs with Dex and LPS and co-cultured with T-cells from OT-I or OT-II transgenic mice. The induction of apoptosis in T-cells was highly reduced using the Lcn2-/- compared to WT DCs. In vivo Cytotoxic T-Lymphocyte killing assay using LPS treated Lcn2-/-- or WT-DCs as immunisation showed that the specific killing ability was diminished in mice that had received Lcn2-/--DCs (in WT-DCs 96,18 ± 0,5057, in Lcn2-/--DCs 87,12 ± 2,034, p<0.01). Further we observed that LCN2 is involved in the priming of CD8+ and CD4+ T-cells in a dose dependant manner, and it induces a TH1 microenvironment. In DCs treated with Dex and LPS high expression of LCN2 is involved in CD8+ T-cell apoptosis. This study aims to contribute to better understand the DCs’ biology and to improve their use in cancer immune therapy. Keywords: LCN2, DCs, Dex, microenvironment, Immunisation Conference: 15th International Congress of Immunology (ICI), Milan, Italy, 22 Aug - 27 Aug, 2013. Presentation Type: Abstract Topic: Translational immunology and immune intervention Citation: Floderer M, Prchal M and Vizzardelli C (2013). Lcn2 secreted from DCs induces CD8+ T-cell apoptosis, it is involved in T-cell priming, and upon DCs immunisation triggers a Th1 phenotype. Front. Immunol. Conference Abstract: 15th International Congress of Immunology (ICI). doi: 10.3389/conf.fimmu.2013.02.00732 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 13 Jun 2013; Published Online: 22 Aug 2013. * Correspondence: Dr. Caterina Vizzardelli, St.Anna Children's Cancer Research Institute, Tumour Immunology, Vienna, Austria, 1090, Austria, caterina.vizzardelli@gmail.com Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract Supplemental Data The Authors in Frontiers Melanie Floderer Michaela Prchal Caterina Vizzardelli Google Melanie Floderer Michaela Prchal Caterina Vizzardelli Google Scholar Melanie Floderer Michaela Prchal Caterina Vizzardelli PubMed Melanie Floderer Michaela Prchal Caterina Vizzardelli Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.