title: An inflammatory link in atherosclerosis and obesity. Co-stimulatory molecules.
abstract: Atherosclerosis and obesity-induced metabolic dysfunction are lipid-driven inflammatory pathologies responsible for a major part of cardiovascular complications. Immune cell activation as well as interactions between the different immune cells is dependent on and controlled by a variety of co-stimulatory signals. These co-stimulatory signals can either aggravate or ameliorate the disease depending on the stage of the disease, the cell-types involved and the signal transduction cascades initiated. This review focuses on the diverse roles of the most established co-stimulatory molecules of the B7 and Tumor Necrosis Factor Receptor (TNFR) families, ie the CD28/CTLA4-CD80/CD86 and CD40L/CD40 dyads in the pathogenesis of atherosclerosis and obesity. In addition, we will explore their potential as therapeutic targets in both atherosclerosis and obesity.
authors.affiliation: Prof. Andreas Zirlik, Atherogenesis Research Group, Heart Center Freiburg University, Cardiology and Angiology I, University of Freiburg, Germany, E-mail: andreas.zirlik@uniklinik-freiburg.de.
authors.forename: A
authors.initials: A
authors.lastname: Zirlik
authors.forename: E
authors.initials: E
authors.lastname: Lutgens
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000276:immunology*; D016207:Cytokines / Q000276:immunology*; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology*; D018836:Inflammation Mediators / Q000276:immunology*; D050356:Lipid Metabolism / Q000276:immunology*; D018448:Models, Immunological; D009765:Obesity / Q000276:immunology*; D015398:Signal Transduction / Q000276:immunology
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators
keywords: Atherosclerosis; co-stimulation; obesity