title: Targeting B cells in atherosclerosis: closing the gap from bench to bedside.
abstract: Atherosclerotic plaque formation is strongly influenced by different arms of the immune system, including B lymphocytes. B cells are divided into 2 main families: the B1 and the B2 cells. B1 cells are atheroprotective mainly via the production of natural IgM antibodies that bind oxidized low-density lipoprotein and apoptotic cells. B2 cells, which include follicular and marginal zone B cells, are suggested to be proatherogenic. Antibody-mediated depletion of B cells has become a valuable treatment option for certain autoimmune diseases, such as systemic lupus erythematosus and rheumatoid arthritis that are also characterized by the development of premature atherosclerosis. Thus, B cells represent a novel interesting target for therapeutic modulation of the atherosclerotic disease process. Here, we discuss the effect of different of B-cell subsets in experimental atherosclerosis, their mechanism of action as well as potential ways to exploit these findings for the treatment of human disease.
authors.affiliation: From the Department of Laboratory Medicine, Medical University of Vienna and Center for Molecular Medicine (CeMM) of the Austrian Academy of Sciences, Vienna, Austria (D.T., C.J.B.); and Division of Cardiovascular Medicine, Department of Medicine, University of Cambridge, Cambridge, United Kingdom (A.P.S., Z.M.).
authors.forename: Dimitrios
authors.initials: D
authors.lastname: Tsiantoulas
authors.affiliation: From the Department of Laboratory Medicine, Medical University of Vienna and Center for Molecular Medicine (CeMM) of the Austrian Academy of Sciences, Vienna, Austria (D.T., C.J.B.); and Division of Cardiovascular Medicine, Department of Medicine, University of Cambridge, Cambridge, United Kingdom (A.P.S., Z.M.).
authors.forename: Andrew P
authors.initials: AP
authors.lastname: Sage
authors.affiliation: From the Department of Laboratory Medicine, Medical University of Vienna and Center for Molecular Medicine (CeMM) of the Austrian Academy of Sciences, Vienna, Austria (D.T., C.J.B.); and Division of Cardiovascular Medicine, Department of Medicine, University of Cambridge, Cambridge, United Kingdom (A.P.S., Z.M.).
authors.forename: Ziad
authors.initials: Z
authors.lastname: Mallat
authors.affiliation: From the Department of Laboratory Medicine, Medical University of Vienna and Center for Molecular Medicine (CeMM) of the Austrian Academy of Sciences, Vienna, Austria (D.T., C.J.B.); and Division of Cardiovascular Medicine, Department of Medicine, University of Cambridge, Cambridge, United Kingdom (A.P.S., Z.M.). christoph.binder@meduniwien.ac.at.
authors.forename: Christoph J
authors.initials: CJ
authors.lastname: Binder
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D016175:B-Lymphocyte Subsets / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D004195:Disease Models, Animal; D006801:Humans; D007155:Immunologic Factors / Q000627:therapeutic use*; D018836:Inflammation Mediators / Q000276:immunology / Q000378:metabolism; D058990:Molecular Targeted Therapy; D009203:Myocardial Infarction / Q000188:drug therapy / Q000276:immunology / Q000378:metabolism; D010641:Phenotype; D015398:Signal Transduction / Q000187:drug effects; D057170:Translational Research, Biomedical
chemical_list: D007155:Immunologic Factors; D018836:Inflammation Mediators
keywords: B lymphocytes; B-cell activating factor; antibodies; atherosclerosis; belimumab; cardiovascular diseases; rituximab