title: Treating atherosclerosis with regulatory T cells.
abstract: Regulatory T cells (Tregs) play an important role in the regulation of T-cell-mediated immune responses through suppression of T-cell proliferation and secretion of inhibitory cytokines, such as interleukin-10 and transforming growth factor-β. Impaired Treg numbers and function have been associated with numerous diseases, and an imbalance between proinflammatory/proatherogenic cells and Tregs promotes atherosclerotic disease. Restoration of this balance by inducing Tregs has great therapeutic potential to prevent cardiovascular disease. In addition to suppressing differentiation and function of effector T cells, Tregs have been shown to induce anti-inflammatory macrophages, inhibit foam cell formation and to influence cholesterol metabolism. Furthermore, Tregs suppress immune responses of endothelial cells and innate lymphoid cells. In this review, we focus on the recent knowledge on Treg subsets, their activity and function in atherosclerosis, and discuss promising strategies to use Tregs as a therapeutic tool to prevent cardiovascular disease.
authors.affiliation: From the Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA (A.C.F., A.H.L.); and Division of Biopharmaceutics, Leiden Academic Centre for Drug Research, Leiden University, Gorlaeus Laboratories, Leiden, The Netherlands (J.K.).
authors.forename: Amanda C
authors.initials: AC
authors.lastname: Foks
authors.affiliation: From the Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA (A.C.F., A.H.L.); and Division of Biopharmaceutics, Leiden Academic Centre for Drug Research, Leiden University, Gorlaeus Laboratories, Leiden, The Netherlands (J.K.).
authors.forename: Andrew H
authors.initials: AH
authors.lastname: Lichtman
authors.affiliation: From the Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA (A.C.F., A.H.L.); and Division of Biopharmaceutics, Leiden Academic Centre for Drug Research, Leiden University, Gorlaeus Laboratories, Leiden, The Netherlands (J.K.). j.kuiper@lacdr.leidenuniv.nl.
authors.forename: Johan
authors.initials: J
authors.lastname: Kuiper
mesh_terms: D019264:Adoptive Transfer; D000818:Animals; D050197:Atherosclerosis / Q000276:immunology / Q000378:metabolism / Q000473:pathology / Q000628:therapy*; D003713:Dendritic Cells / Q000276:immunology / Q000378:metabolism; D006801:Humans; D007111:Immunity, Cellular / Q000187:drug effects*; D007155:Immunologic Factors / Q000627:therapeutic use*; D007249:Inflammation / Q000276:immunology / Q000378:metabolism / Q000473:pathology / Q000628:therapy*; D018836:Inflammation Mediators / Q000276:immunology / Q000378:metabolism; D008213:Lymphocyte Activation / Q000187:drug effects; D008264:Macrophages / Q000276:immunology / Q000378:metabolism; D010641:Phenotype; D015398:Signal Transduction / Q000187:drug effects; D050378:T-Lymphocytes, Regulatory / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism / Q000637:transplantation*
chemical_list: D007155:Immunologic Factors; D018836:Inflammation Mediators
keywords: atherosclerosis; immune system