13 research outputs found
Procedural theory - accomplishing design goals
Landscaping is the act of taking a piece of land and analysing, evaluating, and beautifying it, while focusing on maintaining and increasing sustainability, functionality, and usability for people in a resource-effective way.
The course Urban Landscape Design (LK0400) is a bachelor’s level course focusing on design of urban green spaces, offered at the Swedish University of Agricultural Sciences, and run by the Department of Landscape Architecture, Planning and Management (LTV faculty). The course is run as a stand-alone course for national and international students and as a programme course in the Landscape Engineer Programme at Uppsala and Alnarp, and in the Garden Design, Landscape Engineer Programme at Alnarp
Particle size and surface charge affect particle uptake by human dendritic cells in an in vitro model
Interaction of dendritic cells with antigen-containing liposomes: effect of bilayer composition
Cytotoxic T-lymphocyte antigen-4 microsatellite polymorphism is associated with multiple myeloma
Expression of the Epstein-Barr Virus-Encoded Epstein-Barr Virus Nuclear Antigen 1 in Hodgkin’s Lymphoma Cells Mediates Up-Regulation of CCL20 and the Migration of Regulatory T Cells
In ∼50% of patients with Hodgkin’s lymphoma (HL), the Epstein-Barr virus (EBV), an oncogenic herpesvirus, is present in tumor cells. After microarray profiling of both HL tumors and cell lines, we found that EBV infection increased the expression of the chemokine CCL20 in both primary Hodgkin and Reed-Sternberg cells and Hodgkin and Reed-Sternberg cell-derived cell lines. Additionally, this up-regulation could be mediated by the EBV nuclear antigen 1 protein. The higher levels of CCL20 in the supernatants of EBV-infected HL cell lines increased the migration of CD4+ lymphocytes that expressed FOXP3, a marker of regulatory T cells (Tregs), which are specialized CD4+ T cells that inhibit effector CD4+ and CD8+ T cells. In HL, an increased number of Tregs is associated with the loss of EBV-specific immunity. Our results identify a mechanism by which EBV can recruit Tregs to the microenvironment of HL by inducing the expression of CCL20 and, by doing so, prevent immune responses against the virus-infected tumor population. Further investigation of how EBV recruits and modifies Tregs will contribute not only to our understanding of the pathogenesis of virus-associated tumors but also to the development of therapeutic strategies designed to manipulate Treg activity